it seems charlene is the first one to survive vCJD

ORIGINAL: ErEf

Ray,

I know you take this personal and you stand up for the ingorant one.. the minors etc.

But please do not insult Mike and of course that counts for everyone. Don't lose your temper as if your brain is allready affected.

ontopic

Agreed, sorry Ray!

o/t!

Ok, since I proved that your disease is not an issue in our country, you are now attempting to change your original argument?

Dear Mr MCCandles, What do you mean with "no victim in the USA?".

This article proves you are wrong:

Published on Wednesday, January 7, 2004 by CommonDreams.org
Could Mad Cow Disease Already be Killing Thousands of Americans Every Year?
by Michael Greger, M.D.

October 2001, 34-year-old Washington State native Peter Putnam started losing his mind. One month he was delivering a keynote business address, the next he couldn't form a complete sentence. Once athletic, soon he couldn't walk. Then he couldn't eat. After a brain biopsy showed it was Creutzfeldt-Jakob disease, his doctor could no longer offer any hope. "Just take him home and love him," the doctor counseled his family.[1,2,3] Peter's tragic death, October 2002, may have been caused by Mad Cow disease.

Seven years earlier and 5000 miles away, Stephen Churchill was the first in England to die. His first symptoms of depression and dizziness gave way to a living nightmare of terrifying hallucinations; he was dead in 12 months at age 19.[4] Next was Peter Hall, 20, who showed the first signs of depression around Christmas, 1994. By the next Christmas, he couldn't walk, talk, or do anything for himself.[5] Then it was Anna's turn, then Michelle's. Michelle Bowen, age 29, died in a coma three weeks after giving birth to her son via emergency cesarean section. Then it was Alison's turn. These were the first five named victims of Britain's Mad Cow epidemic. They died from what the British Secretary of Health called the worst form of death imaginable, Creutzfeldt-Jakob disease, a relentlessly progressive and invariably fatal human dementia.[6] The announcement of their deaths, released on March 20, 1996 (ironically, Meatout Day[7]), reversed the British government's decade-old stance that British beef was safe to eat.[8]

It is now considered an "incontestable fact" that these human deaths in Britain were caused by Bovine Spongiform Encephalopathy (BSE), or Mad Cow disease.[9] Bovine means "cow or cattle," spongiform means "sponge-like," and encephalopathy means "brain disease." Mad Cow disease is caused by unconventional pathogens called prions--literally infectious proteins--which, because of their unique structure, are practically invulnerable, surviving even incineration[10] at temperatures hot enough to melt lead.[11] The leading theory as to how cows got Mad Cow disease in the first place is by eating diseased sheep infected with a sheep spongiform encephalopathy called scrapie.[12]

In humans, prions can cause Creutzfeldt-Jakob disease (CJD), a human spongiform encephalopathy whose clinical picture can involve weekly deterioration into blindness and epilepsy as one's brain becomes riddled with tiny holes.

We've known about Creutzfeldt-Jakob disease for decades, since well before the first mad cow was discovered in 1985. Some cases of CJD seemed to run in families; other cases seemed to just arise spontaneously in about one in a million people every year, and were hence dubbed "sporadic." The new form of CJD caused by eating beef from cows infected with Mad Cow disease, though, seemed to differ from the classic sporadic CJD.

The CJD caused by infected meat has tended to strike younger people, has produced more psychotic symptoms, and has often dragged on for a year or more. The most defining characteristic, though, was found when their brains were sampled. The brain pathology was vividly reminiscent of Kuru, a disease once found in a New Guinea tribe of cannibals who ate the brains of their dead.[13] Scientists called this new form of the disease "variant" CJD.

Other than Charlene, a 24 year old woman now so tragically dying in Florida, who was probably infected in Britain, there have been no reported cases of variant CJD in the U.S.[14] Hundreds of confirmed cases of the sporadic form of Creutzfeldt-Jakob disease, however, arise in the United States every year,[15] but the beef industry is quick to point out these are cases of sporadic CJD, not the new variant known to be caused by Mad Cow disease.[16] Of course, no one knows what causes sporadic CJD. New research, discussed below, suggests that not hundreds but thousands of Americans die of sporadic CJD every year, and that some of these CJD deaths may be caused by eating infected meat after all.

Although the fact that Mad Cow disease causes variant CJD had already been strongly established, researchers at the University College of London nevertheless created transgenic mice complete with "humanized" brains genetically engineered with human genes to try to prove the link once and for all. When the researchers injected one strain of the "humanized" mice with infected cow brains, they came down with the same brain damage seen in human variant CJD, as expected. But when they tried this in a different strain of transgenic "humanized" mice, those mice got sick too, but most got sick from what looked exactly like sporadic CJD! The Mad Cow prions caused a disease that had a molecular signature indistinguishable from sporadic CJD. To the extent that animal experiments can simulate human results, their shocking conclusion was that eating infected meat might be responsible for some cases of sporadic CJD in addition to the expected variant CJD. The researchers concluded that "it is therefore possible that some patients with [what looks like]... sporadic CJD may have a disease arising from BSE exposure."[17] Laura Manuelidis, section chief of surgery in the neuropathology department at Yale University comments, "Now people are beginning to realize that because something looks like sporadic CJD they can't necessarily conclude that it's not linked to [Mad Cow disease]..."[18]

This is not the first time meat was linked to sporadic CJD. In 2001, a team of French researchers found, to their complete surprise, a strain of scrapie--"mad sheep" disease--that caused the same brain damage in mice as sporadic CJD.[19] "This means we cannot rule out that at least some sporadic CJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory.[20]

Population studies had failed to show a link between CJD and lamb chops, but this French research provided an explanation why. There seem to be six types of sporadic CJD and there are more than 20 strains of scrapie. If only some sheep strains affect only some people, studies of entire populations may not clearly show the relationship. Monkeys fed infected sheep brains certainly come down with the disease.[21] Hundreds of "mad sheep" were found in the U.S. in 2003.[22] Scrapie remains such a problem in the United States that the USDA has issued a scrapie "declaration of emergency."[23] Maybe some cases of sporadic CJD in the U.S. are caused by sheep meat as well.[24]

Pork is also a potential source of infection. Cattle remains are still boiled down and legally fed to pigs (as well as chickens) in this country. The FDA allows this exemption because no "naturally occurring" porcine (pig) spongiform encephalopathy has ever been found. But American farmers typically kill pigs at just five months of age, long before the disease is expected to show symptoms. And, because pigs are packed so tightly together, it would be difficult to spot neurological conditions like spongiform encephalopathies, whose most obvious symptoms are movement and gait disturbances. We do know, however, that pigs are susceptible to the disease--laboratory experiments show that pigs can indeed be infected by Mad Cow brains[25]--and hundreds of thousands of downer pigs, too sick or crippled by injury to even walk, arrive at U.S. slaughterhouses every year.[26]

A number of epidemiological studies have suggested a link between pork consumption and sporadic CJD. Analyzing peoples' diet histories, the development of CJD was associated with eating roast pork, ham, hot dogs, pork chops, smoked pork, and scrapple (a kind of pork pudding made from various hog carcass scraps). The researchers concluded, "The present study indicated that consumption of pork as well as its processed products (e.g., ham, scrapple) may be considered as risk factors in the development of Creutzfeldt-Jakob disease." Compared to people that didn't eat ham, for example, those who included ham in their diet seemed ten times more likely to develop CJD.[27] In fact, the USDA may have actually recorded an outbreak of "mad pig" disease in New York 25 years ago, but still refuses to reopen the investigation despite petitions from the Consumer's Union (the publishers of Consumer Reports magazine).[28]

Sporadic CJD has also been associated with weekly beef consumption,[29] as well as the consumption of roast lamb,[30] veal, venison, brains in general,[31] and, in North America, seafood.[32,33] The development of CJD has also, surprisingly, been significantly linked to exposure to animal products in fertilizer,[34] sport fishing and deer hunting in the U.S.,[35] and frequent exposure to leather products.[36]

We do not know at this time whether chicken meat poses a risk. There was a preliminary report of ostriches allegedly fed risky feed in German zoos who seemed to come down with a spongiform encephalopathy.[37] Even if chickens and turkeys themselves are not susceptible, though, they may become so-called "silent carriers" of Mad Cow prions and pass them on to human consumers.[38] Dateline NBC quoted D. Carleton Gajdusek, the first to be awarded a Nobel Prize in Medicine for his work on prion diseases,[39] as saying, "it's got to be in the pigs as well as the cattle. It's got to be passing through the chickens."[40] Dr. Paul Brown, medical director for the US Public Health Service, believes that pigs and poultry could indeed be harboring Mad Cow disease and passing it on to humans, adding that pigs are especially sensitive to the disease. "It's speculation," he says, "but I am perfectly serious."[41]

The recent exclusion of most cow brains, eyes, spinal cords, and intestines from the human food supply may make beef safer, but where are those tissues going? These potentially infectious tissues continue to go into animal feed for chickens, other poultry, pigs, and pets (as well as being rendered into products like tallow for use in cosmetics, the safety of which is currently under review[42]). Until the federal government stops the feeding of slaughterhouse waste, manure, and blood to all farm animals, the safety of meat in America cannot be guaranteed.

The hundreds of American families stricken by sporadic CJD every year have been told that it just occurs by random chance. Professor Collinge, the head of the University College of London lab, noted "When you counsel those who have the classical sporadic disease, you tell them that it arises spontaneously out of the blue. I guess we can no longer say that."

"We are not saying that all or even most cases of sporadic CJD are as a result of BSE exposure," Professor Collinge continued, "but some more recent cases may be--the incidence of sporadic CJD has shown an upward trend in the UK over the last decade... serious consideration should be given to a proportion of this rise being BSE-related. Switzerland, which has had a substantial BSE epidemic, has noted a sharp recent increase in sporadic CJD."[43] In the Nineties, Switzerland had the highest rate of Mad Cow disease in continental Europe, and their rate of sporadic CJD doubled.[44]

We don't know exactly what's happening to the rate of CJD in this country, in part because CJD is not an officially notifiable illness.[45] Currently only a few states have such a requirement. Because the Centers for Disease Control (CDC) does not actively monitor the disease on a national level,[46] a rise similar to the one in Europe could be missed.[47] In spite of this, a number of U.S. CJD clusters have already been found. In the largest known U.S. outbreak of sporadic cases to date,[48] five times the expected rate was found to be associated with cheese consumption in Pennsylvania's Lehigh Valley.[49] A striking increase in CJD over expected levels was also reported in Florida[50] and New York (Nassau County)[51] with anecdotal reports of clusters of deaths in Oregon[52] and New Jersey.[53]

Perhaps particularly worrisome is the seeming increase in CJD deaths among young people in this country. In the 18 years between 1979 and 1996, only a single case of sporadic CJD was found in someone under 30. Whereas between 1997 and 2001, five people under 30 died of sporadic CJD. So five young Americans dying in five years, as opposed to one young case in the previous 18 years. The true prevalence of CJD among any age group in this country remains a mystery, though, in part because it is so commonly misdiagnosed.[54]

The most frequent misdiagnosis of CJD among the elderly is Alzheimer's disease.[55] Neither CJD nor Alzheimer's can be conclusively diagnosed without a brain biopsy,[56] and the symptoms and pathology of both diseases overlap. There can be spongy changes in Alzheimer's, for example, and senile Alzheimer's plaques in CJD.[57] Stanley Prusiner, the scientist who won the Nobel Prize for his discovery of prions, speculates that Alzheimer's may even turn out to be a prion disease as well.[58] In younger victims, CJD is more often misdiagnosed as multiple sclerosis or as a severe viral infection.[59]

Over the last 20 years the rates of Alzheimer's disease in the United States have skyrocketed.[60] According to the CDC, Alzheimer's Disease is now the eighth leading cause of death in the United States,[61] afflicting an estimated 4 million Americans.[62] Twenty percent or more of people clinically diagnosed with Alzheimer's disease, though, are found at autopsy not to have had Alzheimer's at all.[63] A number of autopsy studies have shown that a few percent of Alzheimer's deaths may in fact be CJD. Given the new research showing that infected beef may be responsible for some sporadic CJD, thousands of Americans may already be dying because of Mad Cow disease every year.[64]

Nobel Laureate Gajdusek, for example, estimates that 1% of people showing up in Alzheimer clinics actually have CJD.[65] At Yale, out of a series of 46 patients clinically diagnosed with Alzheimer's, six were proven to have CJD at autopsy.[66] In another study of brain biopsies, out of a dozen patients diagnosed with Alzheimer's according to established criteria, three of them were actually dying from CJD.[67] An informal survey of neuropathologists registered a suspicion that CJD accounts for 2-12% of all dementias in general.[68] Two autopsy studies showed a CJD rate among dementia deaths of about 3%.[69,70] A third study, at the University of Pennsylvania, showed that 5% of patients diagnosed with dementia had CJD.[71] Although only a few hundred cases of sporadic CJD are officially reported in the U.S. annually,[72] hundreds of thousands of Americans die with dementia every year.[73] Thousands of these deaths may actually be from CJD caused by eating infected meat.

The incubation period for human spongiform encephalopathies such as CJD can be decades.[74] This means it can be years between eating infected meat and getting diagnosed with the death sentence of CJD. Although only about 150 people have so far been diagnosed with variant CJD worldwide, it will be many years before the final death toll is known. In the United States, an unknown number of animals are infected with Mad Cow disease, causing an unknown number of human deaths from CJD. The U.S. should immediately begin testing all cows destined for human consumption, as is done in Japan, should stop feeding slaughterhouse waste to all farm animals (see http://organicconsumers.org/madcow/GregerBSE.cfm), and should immediately enact an active national surveillance program for CJD.[75]

Five years ago this week, the Center for Food Safety, the Humane Farming Association, the Center for Media & Democracy, and ten families of CJD victims petitioned the FDA and the CDC to immediately enact a national CJD monitoring system, including the mandatory reporting of CJD in all 50 states.[76] The petition was denied.[77] The CDC argued that their passive surveillance system tracking death certificate diagnoses was adequate. Their analysis of death certificates in three states and two cities, for example, showed an overall stable and typical one in a million CJD incidence rate from 1979 to 1993.[78] But CJD is so often misdiagnosed, and autopsies are so infrequently done, that this system may not provide an accurate assessment.[79]

In 1997, the CDC set up the National Prion Disease Pathology Surveillance Center at Case Western Reserve University to analyze brain tissue from CJD victims in the U.S. in hopes of tracking any new developments. In Europe, surveillance centers have been seeing most, if not all, cases of CJD. The U.S. center sees less than half. "I'm very unhappy with the numbers," laments Pierluigi Gambetti , the director of the Center. "The British and Germans politely smile when they see we examine 30% or 40% of the cases," he says. "They know unless you examine 80% or more, you are not in touch."[80] "The chance of losing an important case is high."[81]

One problem is that many doctors don't even know the Center exists. And neither the CDC nor the Center are evidently authorized to reach out to them directly to bolster surveillance efforts, because it's currently up to each state individually to determine how--or even whether--they will track the disease. In Europe, in contrast, the national centers work directly with each affected family and their physicians.[82] In the U.S., most CJD cases--even the confirmed ones--seem to just fall through the cracks. In fact, based on the autopsy studies at Yale and elsewhere, it seems most CJD cases in the U.S. aren't even picked up in the first place.

Autopsy rates have dropped in the U.S. from 50% in the Sixties to less than 10% at present.[83] Although one reason autopsies are rarely performed on atypical dementia cases is that medical professionals are afraid of catching the disease,[84] the primary reason for the decline in autopsy rates in general appears to be financial. There is currently no direct reimbursement to doctors or hospitals for doing autopsies, which often forces the family to absorb the cost of transporting the body to an autopsy center and having the brain samples taken, a tab that can run upwards of $1500.[85]

Another problem is that the National Prion Disease Pathology Surveillance Center itself remains underfunded. Paul Brown, medical director for the National Institutes of Health, has described the Center's budget as "pitiful," complaining that "there isn't any budget for CJD surveillance."[86] To adequately survey America's 290 million residents, "you need a lot of money." UK CJD expert Robert Will explains, "There was a CJD meeting of families in America in which... [the CDC] got attacked fairly vigorously because there wasn't proper surveillance. You could only do proper surveillance if you have adequate resources."[87] "I compare this to the early days of AIDS," says protein chemist Shu Chen, who directs the Center's lab, "when no one wanted to deal with the crisis."[88]

Andrew Kimbrell, the director of the Center for Food Safety, a D.C.-based public interest group, writes, "Given what we know now, it is unconscionable that the CDC is not strictly monitoring these diseases."[89] Given the presence of Mad Cow disease in the U.S., we need to immediately enact uniform active CJD surveillance on a national level, provide adequate funding not only for autopsies but also for the shipment of bodies, and require mandatory reporting of the disease in all 50 states. In Britain, even feline spongiform encephalopathy, the cat version of Mad Cow disease, is an officially notifiable illness. "No one has looked for CJD systematically in the U.S.," notes NIH medical director Paul Brown. "Ever."[90]

The animal agriculture industries continue to risk public safety, and the government seems to protect the industries' narrow business interests more than it protects its own citizens. Internal USDA documents retrieved through the Freedom of Information Act show that our government did indeed consider a number of precautionary measures as far back as 1991 to protect the American public from Mad Cow disease. According to one such document, however, the USDA explained that the "disadvantage" of these measures was that "the cost to the livestock and rendering industries would be substantial."[91]

Plant sources of protein for farm animals can cost up to 30% more than cattle remains.[92] The Cattlemen's Association admitted a decade ago that animal agribusiness could indeed find economically feasible alternatives to feeding slaughterhouse waste to other animals, but that the they did not want to set a precedent of being ruled by "activists."[93]

Is it a coincidence that USDA Secretary Veneman chose Dale Moore, former chief lobbyist for the National Cattlemen's Beef Association, as her chief of staff?[94] Or Alison Harrison, former director of public relations for the Cattlemen's Association, as her official spokeswoman?[95] Or that one of the new Mad Cow committee appointees is William Hueston, who was paid by the beef industry to testify against Oprah Winfrey in hopes of convicting her of beef "disparagement"?[96] After a similar conflict of interest unfolded in Britain, their entire Ministry of Agriculture was dissolved and an independent Food Safety Agency was created, whose sole responsibility is to protect the public's health. Until we learn from Britain's lesson, and until the USDA stops treating this as a PR problem to be managed instead of a serious global threat,[97] millions of Americans will remain at risk.

Michael Greger, M.D., has been the Chief BSE Investigator for Farm Sanctuary since 1993 and the Mad Cow Coordinator for the Organic Consumers Association since 2001.

For periodic updates on the Mad Cow crisis send a blank email to DrGregerMadCowUpdates-subscribe@lists.riseup.net



REFERENCES:

(Full text of specific articles available by emailing article-request@DrGreger.org)

1 Spokesman Review. 22 September 2003 http://www.organicconsumers.org/madcow/putnam92203.cfm

2 HealthDayNews. 26 September 2003 http://www.healthday.com/view.cfm?id=515265

3 Reuters. 27 December 2003 http://www.organicconsumers.org/madcow/cjd122703.cfm

4 Moyes, Jojo. "Depression Leads to Painful Death." Independent 21 March 1996: 1.

5 "Victims' Families Cry Cover-Up by Protecting Beef Industry, Government Cost Lives, They Say." Miami Herald 26 March 1996: 7A.

6 PA News 30 November 1998.

7 http://meatout.org/

8 Brown, Paul. "Beef Crisis." Guardian 26 March 1996a: 7.

9 British Medical Journal 322(2001):841.

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11 Bentor, Yinon. Chemical Element.com - Lead. Jun. 3, 2003. http://www.chemicalelements.com/elements/pb.html

12 British Medical Journal 322(2001):841.

13 Bulletin of the World Health Organization 70 (1992): 183- 190.

14 http://www.organicconsumers.org/madcow/florida1304.cfm

15 Journal of the American Medical Association, November 8, 2000; 284(18).

16 http://www.bseinfo.org/dsp/dsplocationContent.cfm?locationId=1267

17 "BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein." EMBO Journal, Vol. 21, No. 23, 6358-6368, 2002. http://emboj.oupjournals.org/cgi/content/full/21/23/6358

18 United Press International. 29 December 2003. http://organicconsumers.org/madcow/CJD122903.cfm

19 Proceedings of the National Academy of Sciences 98(2001):4142.

20 "BSE may cause more CJD cases than thought New Scientist 28 November 2002.

21 Journal of Infectious Disease 142(1980):205-8.

22 http://www.aphis.usda.gov/vs/nahps/scrapie/yearly_report/yearly-report.html

23 March 17, 2000 Federal Register (Volume 65,age 14521). http://www.mad-cow.org/00/apr00scrapie.html

24 "Sheep consumption: a possible source of spongiform encephalopathy in humans." Neuroepidemiology. 4(1985):240-9.

25 The Veterinary Record 127(1990):338.

26 National Hog Farmer. 15 February 2002.

27 American Journal of Epidemiology Vol. 122, No. 3 (1985), pgs. 443-451.

28 http://www.consumersunion.org/food/psecpi301.htm

29 Creutzfeldt-Jakob disease surveillance in the UK: sixth annual report 1997. Edinburgh, Scotland: National CJD Surveillance Unit, 1998.

30 American Journal of Epidemiology Vol. 122, No. 3 (1985), pgs. 443-451.

31 Creutzfeldt-Jakob disease surveillance in the UK: sixth annual report 1997. Edinburgh, Scotland: National CJD Surveillance Unit, 1998.

32 Quarterly Journal of Medicine 93(2000):617.

33 American Journal of Epidemiology 98( 1973):381-394.

34 Lancet 1998; 351:1081-5.

35 American Journal of Epidemiology 122(1985)443-451.

36 Lancet 1998; 351:1081-5.

37 Schoon, H.A., Brunckhorst, D. and Pohlenz J. (1991) Spongiform Encephalopathy in a Red-Necked Ostrich, Tierartzliche Praxis, 19, 263-5

38 Journal of Virology 75(21):10073-89 (2001).

39 http://www.nobel.se/medicine/laureates/1976/gajdusek-lecture.html

40 NBC Dateline 14 March 1997.

41 Pearce, Fred. "BSE May Lurk in Pigs and Chickens." New Scientist 6 April 1996: 5.

42 http://organicconsumers.org/madcow/tallow123103.cfm

43 "BSE May Have Caused Some Cases Of CJD As Well As vCJD." The Guardian. 29 November 2002.

44 Lancet 360(2002):139-141.

45 Neuroepidemiology 14 (1995): 174-181.

46 http://www.cdc.gov/ncidod/diseases/cjd/bsecjdqa.htm

47 Altman, Lawrence K. "U.S. Officials Confident That Mad Cow Disease of Britain Has Not Occurred Here." New York Times 27 March 1996: 12A.

48 Flannery, Mary. "Twelve - Fifteen 'Mad Cow' Victims a Year in Area." Philadelphia Daily News 26 March 1996: 03.

49 Neurology 43 (1993): A316.

50 Neurology 44 (1994): A260.

51 Annals of Clinical and Laboratory Science 31(2001):211.

52 Boule, Margie. "Despite Anecdotal Evidence, Docs Say No Mad Cow Disease Here." Oregonian 16 April 1996: C01.

53 Burlington County Times 23 June 2003. http://www.phillyburbs.com/pb-dyn/news/112-06232003-112425.html

54 Philip Yam. The Pathological Protein: Mad Cow, Chronic Wasting, and Other Deadly Prion Diseases. New York: Springer-Verlag Press, 2003

55 British Journal of Psychiatry 158 (1991): 457-70.

56 Neurology 38 (1989): 76-79.

57 Neurology 39 (1989): 1103-1104.

58 New England Journal of Medicine 310 (1984): 661-663.

59 "Brain Disease May Be Commoner Than Thought -Expert." Reuter Information Service 15 May 1996.

60 http://www.cdc.gov/mmwr/preview/mmwrhtml/00001820.htm

61 http://www.cdc.gov/nchs/fastats/alzheimr.htm

62 http://www.nimh.nih.gov/publicat/numbers.cfm

63 Neurology 34 (1984): 939.

64 The Lancet 336 (1990):21.

65 Folstein, M. "The Cognitive Pattern of Familial Alzheimer's Disease." Biological Aspects of Alzheimer's Disease. Ed. R. Katzman. Cold Spring Harbor Laboratory, 1983.

66 Alzheimer Disease and Associated Disorders 2 (1989): 100-109.

67 Teixeira, F., et al. "Clinico-Pathological Correlation in Dementias." Journal of Psychiatry and Neuroscience 20 (1995): 276-282.

68 British Journal of Psychiatry 158 (1991): 457-70.

69 Mahendra, B. Dementia Lancaster: MTP Press Limited, 1987: 174.

70 Archives of Neurology 44 (1987): 24-29.

71 Neurology 38 (1989): 76-79.

72 http://www.cdc.gov/ncidod/diseases/cjd/bsecjdqa.htm

73 Dementia and Normal Aging, Cambridge University Press, 1994.

74 Neurology 55 (2000):1075.

75 Lancet Infectious Disease. 1 August 2003.

76 http://www.mad-cow.org/jan99_petition.html#ddd

77 http://www.centerforfoodsafety.org/li/CDCrspn1.html

78 Morbidity and Mortality Weekly Report 12 April 1996: 295-303.

79 Neurology 43 (1993): A316.

80 The Wall Street Journal. 30 November 2001.

81 Beacon Journal (Akron). 5 June 2001. http://www.organicconsumers.org/madcow/CJD6501.cfm

82 New York Times 30 January 2001.

83 http://abcnews.go.com/sections/living/Healthology/HS_autopsydearth_03130.html

84 Altman, Lawrence K. "Four States Watching for Brain Disorder." New York Times 9 April 1996.

85 http://www.medicomm.net/Consumer%20Site/tp/tp_a15.htm

86 http://www.organicconsumers.org/madcow/fact43001.cfm

87 Case Western Reserve University Magazine - Summer 2001.

88 Case Western Reserve University Magazine - Summer 2001.

89 USA Today. 7 January 1999.

90 Philip Yam. The Pathological Protein: Mad Cow, Chronic Wasting, and Other Deadly Prion Diseases. New York: Springer-Verlag Press, 2003

91 Rampton, S and J. Stauber. Mad Cow USA: Could the Nightmare Happen Here? Common Courage Press; (September 1997):149-50. Full text available free online at http://prwatch.org/books/madcow.html

92 Food Chemical News 25 March 1996: 30.

93 Food Chemical News 5 July 1993: 57-59.

94 http://www.philly.com/mld/inquirer/5884855.htm

95 http://organicconsumers.org/madcow/usda1204.cfm

96 http://www.prwatch.org/prwissues/1998Q1/oprah.html

97 "World Health Organization says BSE is a major threat" http://www.organicconsumers.org/madcow/BSE7601.cfm

Here an interesting article about Mad Pig Disease;


Los Angeles, Califas: An outbreak of "Mad Pig Disease" was reported in El Monte, California on April 1, 1996, by thousands of shocked television viewers. Two Riverside County Sheriff's Deputies had a severe Mad Pig Disease seizure, infecting and rendering extremely ill two Mexican immigrants by the side of the 60 Freeway. The last known major outbreak of Mad Pig Disease in 1991 eventually brought on major inflammation in the entire Los Angeles area.
Scientists at the National Pochismo Institute Centers for Disease Control, who have been studying the epidemic for years, urged the public to take precautions against the disease. Known popularly as Mad Pig Disease, porkus batonus violentus (the formal Latin name) is known to be especially harmful to the physical health and well-being of Chicanos and Mexicanos, although other minority populations have been more at risk in the past.

Carriers Unharmed: MPD is a particularly insidious disease as those who suffer from it do not actually contract the virus, but rather are afflicted by those who do, known as "carriers." Carriers of MPD, almost always law enforcement officers, suffer no harmful consequences from the disease, even after a major seizure such as the one broadcast around the world from El Monte this week.

Symptoms exhibited by carriers include going "hog wild" when apprehending people of color under color of authority. Wild flailing of billy clubs and use of abusive language is also frequent. When carriers of Mad Pig Disease undergo a seizure, nearby civilians may experience severe bruising, or more serious ailments requiring hospitalization or even burial.

Method of Transmission: The Mad Pig virus flourishes in an environment of heated anti-immigrant and anti-minority rhetoric. Proposition 187 and the California Civil Rights Initiative are known agents of transmission for Mad Pig Disease. Other high-risk behavior including Buchananism is also known to induce MPD.

Although carriers are spared any harmful effects and their seizures most often take place at night or within the extra-hospitable incubation arenas of police stations, low-income neighborhoods (where there are likely to be few "credible" observers) and rugged border areas, some have been identified. Known carriers include: Riverside County Sheriff's Deputies Tracy Watson and Kurt Franklin, and LAPD Officers Stacy Koon, Lawrence Powell, and Mark Fuhrman.

Prevention: The National Pochismo Institute Centers for Disease Control reports that the most effective method for citizens to protect themselves from Mad Pig Disease is education. The Centers urged all members of the Chicano and Latino community to learn about the disease and remain vigilant so they do not become victims of an MPD carrier's sudden seizure, as, last week, did two members of the family pictured above.


Treatment: Citizen's Police Review Boards and specialized police training have also been proven to be helpful in combatting this affliction. Infected carriers must be removed from the general badge-wearing population. Those who become ill or injured as a result of exposure to a Mad Pig Disease carrier should report their condition to their local news media and civil rights organizations.

Dear Mr MCCandles, What do you mean with "no victim in the USA?".

This article proves you are wrong:

I'm done with you. I'm not going to respond to your personal rants anymore. You should read your own article before posting:

Other than Charlene, a 24 year old woman now so tragically dying in Florida, who was probably infected in Britain, there have been no reported cases of variant CJD in the U.S.[14]

Raymond, the last post is a joke!


Symptoms exhibited by carriers include going "hog wild" when apprehending people of color under color of authority. Wild flailing of billy clubs and use of abusive language is also frequent. When carriers of Mad Pig Disease undergo a seizure, nearby civilians may experience severe bruising, or more serious ailments requiring hospitalization or even burial.

Method of Transmission: The Mad Pig virus flourishes in an environment of heated anti-immigrant and anti-minority rhetoric . Proposition 187 and the California Civil Rights Initiative are known agents of transmission for Mad Pig Disease. Other high-risk behavior including Buchananism is also known to induce MPD.

Buchanan is a well-known radical right-wing politician.

I think your concerns are valid as well as your wish that Mike should take Secretagogue out of his collection. But you really need to proof read what you've found on the internet!

Although carriers are spared any harmful effects and their seizures most often take place at night or within the extra-hospitable incubation arenas of police stations, low-income neighborhoods (where there are likely to be few "credible" observers) and rugged border areas, some have been identified. Known carriers include: Riverside County Sheriff's Deputies Tracy Watson and Kurt Franklin, and LAPD Officers Stacy Koon, Lawrence Powell, and Mark Fuhrman.

ROFL ..

but his first reply is rather worrying..

you can almost smell the taste of corruption.. and sorry if I say so.. but in that case one supplement seems rather harmless in contrast with what is done in the meat industry.. scarring

They almost know that meat is infected and cases of CJD are more frequent.. better be a vegetarian then.

ORIGINAL: Esperantistino

Raymond, the last post is a joke!


Symptoms exhibited by carriers include going "hog wild" when apprehending people of color under color of authority. Wild flailing of billy clubs and use of abusive language is also frequent. When carriers of Mad Pig Disease undergo a seizure, nearby civilians may experience severe bruising, or more serious ailments requiring hospitalization or even burial.

Method of Transmission: The Mad Pig virus flourishes in an environment of heated anti-immigrant and anti-minority rhetoric . Proposition 187 and the California Civil Rights Initiative are known agents of transmission for Mad Pig Disease. Other high-risk behavior including Buchananism is also known to induce MPD.

Buchanan is a well-known radical right-wing politician.

I think your concerns are valid as well as your wish that Mike should take Secretagogue out of his collection. But you really need to proof read what you've found on the internet!

Raymond, the last post is a joke!

I know, it was posted on 1st of April

I deliberately changed the date to april 5 and left out the pictures, otherwise it was too easy to notice, but since I am already trapped, I will share them with you as well;

[image]local://upfiles/2748/5A3B4F8DA9BA4632A7619DCF7D1B6EFC.jpg[/image]

INS Border Patrol Agents Are Also
Frequently Mad Pig Disease Carriers

[image]local://upfiles/2748/08823E024F134B78B3E736BA0290D863.jpg[/image]

An April MPD Outbreak in Temecula Killed 7



By the way; my post before this one was definately NO joke!
And about that argument between Mr. McCandles and me ; I already gave up taking this guy serious ; like I said; let's agree we never agree. Let him resell whatever he wants to resell; and consumer; inform yourself and beware of what you are buying from whatever fancy website from dangerous resellers. That is the message I finally want to bring.

Attached Image(s)

@Espi

Espi; this article is also not a joke; I decided to post it, because some people of this forum still might think that substance from pig brains are 100% safe; the fact; it is not;

Happy reading;

The case for mad pigs in the US

From the Consumer Policy Institute and Consumers Union: March 24, 1997

Stephen F. Sundlof, D.V.M., Ph.D
Center for Veterinary Medicine
Food and Drug Administration
7500 Standish Place, Room 482, HFV1
RockvLIle, MD 20855

Dear Dr. Sundlof:

We are writing to you to submit information that has recently come to our attention which suggests that a TSElike disease (transmissible spongiform encephalopathy) might exist in pigs in the U.S. We believe this new informantion calls for intensive research and makes it urgent to ban the use of all mammalian proteins, including swine, in the feed of all food animals, until better answers are found.

The evidence for the potential PSE (porcine spongiform encephalopathy ) is as follows. In 1979, an FSQS veternarian, Dr. Masuo Doi, noticed some unusual central nervous system (CNS) symptoms in young (about 6 months old) hogs coming into a slaughter plant In Albany, New York. Since the plant received hogs from a wide variety of sources (New York, Canada, Indiana, Illinois, Ohio, and other Midwestern states) and was not a plant used to dealing with diseased animals, Dr. Doi thought that the problem might be affecting hogs slaughtered nationwide. So, he decided to conduct a detailed study on central nervous system (CNS) symptoms/disease in young hogs coming into that slaughter plant. The study ran for 15 months (January, 1979 to March, 1980) and consisted of extended observations of the behavior of animals with suspected CNS symptoms at the plant, followed by pathological, histopatholpgical, and microbiological work on tissues from various organs of particular animals after slaughter.

For his behavioral observational work, Dr. Doi extended the usual two day observation period to three to four days, during which he took careful notes on the animals' behavior and other vital signs. During the 15 month period of the study, some 106 animals exhibiting CNS symptoms were retained during antemortem inspection.

A 1980 paper that summarized Dr. Doi's findings on the clinical symptoms and incidence of the 'disease," contained descriptions of these symptoms that sound remarkably similar to the symptoms noted for bovine spongiform encephalopathy (BSE):

"Excitable or nervous temperament to external stimuli such as touch to the skin, handling and menacing approach to the animals is a common characteristic sign among swine affected with the disease.... In the advanced stage of the disease, manifestation of neurological signs are evidenced in the form of general ataxia . . . Many animals have been found to be "downers' at first observation; if the hindquarters of these downers are raised they may be able to walk one or two steps and then fall to the ground" (Doi et al., 1980: 2, 4).
Indeed, a table of symptoms includes, for the early stage: "excitability and nervousness (squealing, smacking of lips, grinding of teath, chewing, gnawing ant foaming at mouth); stiffness of limbs . . . 'tic'; weakness of hindquarters; focal tremors of skeletal muscles"; and for the advanced stage: depression; ataxia; crossing over of limbs . . . kneeling posture . . . crawling". In addition to his clinical observations, Dr. Doi also made an 8 mm film of thirteen of the affected animals; film of two of the pigs was shown at the MPI National Pathology Meeting in Seattle, Washington on flay 20, 1979.

Dr. Doi sent tissue samples from suspect cases to the USDA's Eastern Laboratory in Athens, GA for pathological, histopathogical and microbiological work. Known infectious diseases were ruled out. As Dr. Doi points out, "Histopathological studies of tissue collected from the brain and spinal cord of these animals in the early stage of the disease show congestion, hemorrhage and neuronal degeneration. All animals in the advanced stage of the disease have been confined to have Encephalitis or Meningitis by MPI laboratory" (Doi et al., 1980: 5). Eventually some 60 animals were confirmed by the MPI Laboratory to have encephalitis or meningitis, with no ldentifiable cause. As pointed out in a paper presented at the 1979 MPI National Pathology Meetings,


"Since January, a number of hogs in this establishment have been found, in antemortem, to show what appears to be CNS. Sets of tissue samples were sent to the laboratory for examination, various tests were done which include histological study (EH stain), fluorescence antibody technique, virus neutralization and viral and bacteriological isolation. Differential diagnosis was also done to exclude vitamin B deficiency, post vaccination reaction, chlorinated hydrocarbon, arthritis, and transport stress" (Doi et al., 1979).
The brains of the 60 animals were examined. The brain of one of these pigs, on histopathological analysis, exhibited signs reminiscent of a TSE. This histopathological work was performed by Dr. Karl Langheinrich, Pathologist-In-Charge at USDA's Eastern Laboratory in Athens, Georgia. According to the USDA FSQS laboratory report, dated early November, 1979, Dr. Langheinrich noted:


"Microscopic examination of the barrow tissues revealed a encephalopathy and diffuse gliosis characterized by vacuolated neurons, loss of neurons and gliosis in a confined region (nucleus) of the brain stem (anterior ventral midbrain). Only an empty sometimes divided vacuole was present instead of the normal morphology of a nerve cell. Occasionally a shriveled neuron was seen. According to . . . Pathology of Domestic Animals, . . . 'The degeneration of neurons, the reactivity of the glia .... are the classical hallmarks of viral infection of the central nervous system' .... Scrapie of sheep, and encephalopathy of mink, according to the literature, all produce focal vacuolation of the neurons similar to the kind as described for this pig. I was unable to locate any lead as to the cause of this interesting phenomenon in other species including swine'' (Langheinrich, 1979).
Indeed, Dr. Langheinrich's main diagnosis was, " Encephalopathy and diffuse gliosis of undetermined etiology." Portions of the brain were sent for microbiological testing to a neurologist at the University of Georgia, where they came up negative for pseudo-rabies. The brain was unique enough that USDA scientists, such as Dr. Langheinrich and Or. Dot, mentioned it to student and scientific colleagues over the years.

In 1979-1980, BSE was completely unknown. However, both the behavior of the pigs, as well as the histopathology on at least one pig, both showed sign consistent with a porcine TSE. This raises particular concern became the affected animal was only 6 months old; in an animal this young, one would rust expect to see any physical signs of TSE in the brain. Histopathology of TSEs can be very variable, so that spongiform appearance (i.e. vacuolated neurons) are not always present. Behavioral changes can be seen in TSE-infected animals before any changes in brain morphology are visible. Dr. Clarence Gibbs, in testimony before a Congressional hearing on the TSE issue on January 29, 1997 made just this point:

''In the mid-1960s, we demonstrated with our French and English collaborators that during the early incubation of the TSEs, when the virus titer in the brain was very low, there were already marked functional changes, even though no pathology was yet detectable, even ultrastructurally. A month or hero later, polynucleation of neurons appeared in spider monkeys, incubating kuru, and somewhat later, microvacuolation and membrane changes visible only by electron microscopy. This preceded the pest appearance of astrogliosis and spongiform change. It was only much later that the classical scrapieTSE pathology appeared with virus titers in brain of 10 -5 or higher" (Gibbs, 1997; pg. 4).
Given that TSEs can cause behavioral changes in infected animals before any physical changes in the brain can be seen, that the manifestation of TSE in the brain can be quite variable, and that changes in brain morphology are not usually seen in 6 month old animals, we are concerned that the brain of one pig actually showed physical evidence consistent with a TSE.

Following the announcement In March, 1996 of ten cases of new variant CJD (Creutzfeldt-Jakob Disease) in the United Kingdom and their possible connection to BSE, Drs. Doi, Langheinrich and others urged reinvestigation of this case.

In August, 1996, the USDA sent five slides, one of which was a histopathology slide, to Dr. Janice Miller of USDA's Agricultural Research Servicer . Dr. Miller stained four of the slides for prion protein (she didn't stain the H&E slide). Dr. Miller told Consumers Union that Dr. Patrick McCaskey, USDA/FSIS, in charge of the Research Center at Athens, GA, called her, told her that he had five slides that all showed "problems" and asked her to stain four of them. The H&E slide, which clearly show vacuoles in the neurons (one sign of TSE), wasn't stained because to stain for PrP entails removing the slide cover, baking the slide to destain it and then restaining it for PrP; they didn't want to risk destroying the H&E slide.

Dr. Doi had kept frozen samples of the brain and spinal chord of the suspect PSE pig in case the Eastern lab wanted more material for analysis. Unfortunately, these samples were discarded when the packing plant in Albany, NY closed in 1991. It appears that the brain material sent to the Univcrsity of Georgia may have been discarded. [pers com.. Dr. Doi 3/13/97]

Dr. Miller found that the PrP stained in the four pig slides was found only on the inside of neurons, while a positive control slide from a scrapie sheep showed massive amounts of extraneuronal staining. In a letter summarizing her results (copy attached), she concludes that the PrP stained in this pig was normal: "In the pig sections you will see a small particulate type of staining that is confined to neurons and as I indicated on the phone, I would interpret as normal PrP. It is in marked contrast to the massive amount of extraneuronal staining seen in the scrapie section" (Miller, 1996).

Unfortunately, Dr. Miller's finding toes not conclusively rule out a TSE. We are concerned that while British BSE and serapie create a massive amount of extraneuronal staining, there are TSEs where this isn't the case. Three experiments were done in He U.S. -- in Mission, TX (APHIS work), Pullman, Washington (ARS work), and Ames, Iowa (ARS work) -- to see whether sheep scrapie can possibly infect cows. In all the experiments, cattle were inoculated with tissue from scrapie-infected sheep primarily by intra-cranial injection, but in the case of the Texas and Iowa studies also by oral feeding -- to see if cattle were susceptible to scrapie at all. In all three experiments, the majority of cows injected in the brain with scrapie-infected sheep material (usually brains) also developed a fatal spongiform encephalopathy.

However, in all three examples, the symptoms of the spongifonn encephalopathy differed from "mad cow" disease ~ England, as did the appearances of slides from their brains. The brain lesions seen in ail these animals were more variable than those seen in England. When Dr. Miller did similar staining for PrP from these brains (what she called "bovine scrapie") she only found PrP stains on the inside of the neurons, not the massive extraneuronal staining seen in BSE (Miller, pers. comm., March 7, 1997). Thus, Dr. Miller's finding of PrP stains only inside the neurons in the suspect pigs is not particularly reassuring.

In November 1996, USDA sent the single histopathology slide to Dr. William Hadlow, one of the foremost spongiform encephalopathy pathologists in the world. (For unknown reasons, Dr. Hadlow was only sent the one slide; he was not told of the existence of the other slides, nor of Dr. Miller's findings, nor was he told or given the behavioral report from Dr. Doi or the morphology work by Dr. Langheinrich, or shown film of the affected pigs [Dr. Hadlow, pers. com., 3/13/97] From this single slide, Dr. Hadlow found some evidence consistent with TSEs but not enough for a conclusive diagnosis. He noted that the slide contained vacuoles inside neurons, one of the signs of a TSE (Dr. Langheinrich had noted this as well).

However, since such vacuoles occasionally occur normally in pigs, he thought that was not something special: "About twelve (12) neurons in the parasympathetic nucleus have unilocular optically empty vacuoles in the perikaryon. This is the site where such vacuolated neurons have been seen in the swine (as well as in cats and sheep) as an incidental finding. So I do not think such cells have any significance in this pig" (Hadlow, 1996). However, he did see evidence, Including changes in astrocytes, that suggested a TSE, but without examining other parts of the brain to look for other evidence of TSE, he couldn't be sure:


"I am impressed, though, with what seems to be an increase in the number of astrocytes in the section. Some astrocytes are in clusters, some are enlarged and vesicular. Where they are most numerous, a few rod cells (activated microglia) are seen. These findings suggest some perturbation of the nervous tissue. Although such a global response occurs in the transmissible spongifonn encephalopathies, I do no! know its significance in this case without examining other parts of the brain for changes characteristic of these diseases. Thus, from looking; at this one (1) section of brain, I cannot conclude that the pig was affected with a scrapie-like spongiform encephalopathy" (Hadlow, 1996).
In sum, Dr. Hadlow~s letter does not rule out the possibility of a TSE. He says that there is suggestive evidence, but that he would need to look at other slides/sections of the brain, to make a conclusive diagnosis.

In our view, the implications of this data are extremely serious. Experiments in the United Kingdom have shown that pigs are susceptible to BSE. Pigs inoculated with BSE develop a TSE (Dawson et al., 1990). Feeding experiments are underway in the UK to see if BSE can be orally transmitted to pigs; as of March, 1997, some 6 years after the start of the experiment, none of the pigs fed BSE brain have come down with a TSE. Unfortunately the design of this experiment severely limits what we will learn from it, and will most likely not tell us conclusively if pigs can get BSE from feed. It turns out that the pigs were not fed BSE brain continuously. Rather, the pigs were only fed BSE brain material on three days, over a three week period (i.e.. one day each week). Following these three doses, the pigs were never fed contaminated material again. The total amount of infective material given to the pigs was therefore quite small. Thus, a negative finding would be hard to interpret and would not mean that BSE is not orally active in pigs.

We believe that as a top priority USDA should conduct follow-up studies to look for potential CNS/PSE cases in pigs (we plan to communicate about this to USDA separately). In brief, we feel that the following kinds of studies need to be done:

i) TSE pathology experts should examine all the slides from the suspect pig (2709). To our knowledge, at least 12 separate slides exist.

ii) Determine if any brain material from the suspect pig (2709) still exists at the Unlverslty of Georgia. If so, this material should be retrieved and used for transmission studies. In particular, suckling pigs should be inoculated with the material and then permitted to live unto they die of a disease or old age, at which point their brains should be examined for physical signs of a TSE as well as for immunchistochemical evidence (i.e. staining looking for the abnormal PrP).

iii) Increase antemortem inspection for CNS symptoms at hog facilities. Inspectors should be trained to detect the subtle CNS symptoms seen in the Doi et al. study. At a select number of slaughter facilities, animals exhibiting CNS symptoms should be removed and held for observation until they die, at which time their brains should be examined for evidence of a TSE.

iv) Research on CNS symptoms among Me 6,000 or so breeding sows which are permitted to live for 3+ years. Sows exhibiting CNS symptoms should be removed and held for observation until they die, at which time then brains should be exernined for evidence of a TSE.

While such work is underway, given the above inforrnabon, we believe that as a precutionary measure the FDA must expand the proposed ruminant plus mink-to-ruminnant feed ban to prevent protein from any material, including hogs, being fed to any food animal.

Sincerely,

Michael Hansen, Ph.D Research Associate

Jean Halloran Director

References

Dawson, M., Wells, G.A.H., Parker, B.N;J. and A.C Scott. 1990. Primary parental transmission of bovine spongiform encephalopathy to the pig. Veternary Record, pg. 338.

Doi, M., Matzner, N.D. and C. Rothaug. 1979. Observation of CNS disease in market hogs at Est. 893 Tobin Packing Co., Inc. Albany, New York. United States Department of Agriculture, Food Safety and Quality.Service, Meat and Poultry Inspection Service. 7pp.

Doi, M, Langheinrich, K. and F. Rellosa. 1980. Observations of CNS signs in hogs at Est. 893 Tobin Packing C., Inc. Presented by Dr. Lngheinrich at the MPI National Pathology Meeting in Seattle, Washington on July 20, 1979.

Gibbs, C. 1997. Statement to the Committee on Governnent Reform and Oversight, Subcommittee on Human Resources and Intergovernmental Relations, U.S. House of Representatives. January 29,1997.

Hadlow, WJ. 1996. Letter to Patrick McCaskey, USDA/FSIS/Eastem Lab, dated November 13, 1996.

Langheinrich, KA. 1979. USDA/FSQS Laboratory report on specimen 2709. Dated November 8, 1979

Miller, J. 1996. Letter to Patrick McCaskey, USDA/ESIS/Eastern Lab, dated September 6, 1996.

Believe it or not, our farm industry has regulations to prevent such things from happening. We have to trust those laws.

No Mr. Mc Candles; I do not believe you; and I don't trust those US laws either.

Here are the real facts;

What the Meat Industries Don't Want You to Know

I. Prefatory notes
A. Years ago, Dr. Richard Lacey, the University of Leeds microbiologist who
warned about bovine spongiform encephalopathy (BSE) infecting humans in the
U.K. (to much institutional scorn), said, "It is just possible that there is
no mad cow disease in the U.S.A., but I believe it's more likely there is,
but not detected yet." And in 1993, Dr. C.J. Gibbs, former chair of the
World Health Organization's BSE investigation and head of the NIH's brain
studies laboratory, said, "Do I believe BSE is here [in the U.S.]? Of course
I do."

B. The cow who was found to have BSE was more than 6 years old. If she-like
99.5 percent of chickens, pigs, turkeys, and cows in the U.S.-had been
slaughtered before she was 5 years old, you would not have found the disease,
although she would still have had it.

C. Two studies on Alzheimer's victims showed that 5.5 percent and 13
percent, respectively, of patients who had been diagnosed with Alzheimer's
had, in fact, been suffering from the human variant of mad cow disease,
Creutzfeldt-Jakob Disease (CJD). The National Foundation for Infectious
Diseases states that one out of every million people gets CJD, thereby
giving the United States about 270 cases, but if even 1 percent of the 4
million Alzheimer's patients in the U.S. actually have CJD, you would have
40,000 cases, not 270. PETA is calling on the Centers for Disease Control
and Prevention (CDC) to track CJD to determine whether you have an epidemic.

II. The United States Department of Agriculture (USDA) is not protecting
U.S. consumers.

A. The genie has left the bottle. It is better to take steps now than not to
take them, but they are about 10 years too late. The infected cow's brain
was presumably ground up and fed to chickens and pigs who could then be fed
to other cows-practices that are banned in Europe because they allow
transmissible spongiform encephalopathies (TSEs) to jump between species.

B. European scientists recognize that TSEs can jump between species, and
thus, their countries have banned the feeding of animals to animals, but in
the U.S., it remains a legal and universal practice to feed pigs, chickens,
turkey, and fish back to one another, turning natural herbivores into not
just carnivores, but cannibals. Dr. Paul Brown, medical director for the
U.S. Public Health Service, explicitly says that pigs and chickens could
pass TSEs to humans.

C. It is also legal in the U.S. to feed ruminants (i.e., elk, deer, cows,
and sheep) to pigs, chickens, turkeys, and fish and then to feed those
animals back to cows and sheep, who are natural herbivores. Since you know
that sheep, deer, and elk in the U.S. have TSEs, you know that you are
continuing to do exactly what caused this disease in the first place.

D. It is also legal and common for the blood of cows and sheep to be fed to
other cows and sheep (as well as to all the other animals mentioned above).
Humans in the U.S. cannot give blood if they've spent three months or more
in the U.K. since 1980, but cows can still eat other cows' blood in all states in the USA.

E. The one pitiful step taken by the USDA and the U.S. Food and Drug
Administration (FDA) to prevent mad cow disease in the U.S., the widely
popularized 1997 ban on feeding ruminants to ruminants, has not been fully
implemented. In fact, a 2001 FDA investigation found that literally hundreds
of feed suppliers were in violation of the ban.

F. To avoid transmitting mad cow disease to humans, it is illegal in the
United Kingdom to feed any animal who is older than 30 months to humans. In
the U.S., on the other hand, almost all dairy cows, who are the source of
about 40 percent of U.S. hamburger meat, are older than 30 months of age
when they are slaughtered.

III. Grossly inadequate tests for TSEs in animals and humans virtually guarantee that we will not find many cases in the U.S.

A. Pigs, chickens, turkeys, and fish are not tested at all, despite the fact
that they are fed ground up deer, elk, cows, and sheep-as well as other
pigs, chickens, and fish. These animals are then, in turn, ground up and fed
to cows and sheep.

B. Only 20,000 cows were tested last year-out of the 40 million slaughtered
annually, including 130,000 or more downed cattle. (Europe and Japan test
all downed cattle, as recommended by the World Health Organization). And the
USDA cannot even produce the results of the few tests that were conducted.
The infected cow was more than 6 years old. More than 99.5 percent of
animals slaughtered last year were younger than 5 years of age. Considering
the long incubation period, it's a fluke that BSE was found in this cow. No
cows are tested on U.S. farms, where many sick animals die.

C. The tests done in the U.S. involve examining the animals' brains with a
microscope. Considering the long incubation period for the disease (10 to 16
years is the latest estimate for humans) and the fact that no test catches
the disease until it is in its very late stages, it could be a widespread
problem in the U.S., and we wouldn't even know it. The test used by the USDA
is inadequate, which is why the sample from the infected Washington cow had
to be sent to the U.K. to verify that it was BSE-positive.

D. The CDC has not made CJD a notifiable disease, so the disease cannot be
tracked. If a disproportionate number of people were dying of this disease,
we would not even know it. There is some evidence that, in fact, you do have
an epidemic of CJD in the USA, yet the CDC refuses to track it.

IV. Specific lies of the USDA (with thanks to Dr. Michael Greger)

A. The USDA and the meat industry say that BSE cannot be transferred from
mother to calf, but in fact, evidence indicates that it can be. The USDA's
Web site lists the European Commission's official report on maternal
transmission, which concludes, "The results of all epidemiological studies
undertaken to date have been consistent with a rate of maternal risk
enhancement of approximately 10%."

B. The USDA has said that it tests all downed cattle. In fact, there are
about 130,000 downed cattle in the U.S., and only a small fraction are
tested.

C. The USDA and the meat industry say that the U.S. has banned feeding
ruminants to ruminants. In fact, in 2002, the U.S. General Accounting Office
concluded, "BSE may be silently incubating somewhere in the United States.
If that is the case, then FDA's failure to enforce the feed ban may already
have placed U.S. herds and, in turn, the human food supply at risk. FDA has
no clear enforcement strategy for dealing with firms that do not obey the
feed ban. ... Moreover, FDA has been using inaccurate, incomplete, and
unreliable data to track and oversee feed ban compliance." The report can be
downloaded at www.gao.gov/new.items/d02183.pdf.

D. And the biggest whopper of all: The USDA and the meat industry say that
science indicates that muscle can't harbor the infectious agent in TSEs. In
fact, this is not true, according to the CDC and WHO, both of which suggest
that all parts of any contaminated animal pose a risk. Even the USDA's Web
site states, "Epidemiological and case studies have not revealed a common
risk factor among the cases of vCJD. According to the SEAC [the U.K.'s
Spongiform Encephalopathy Advisory Committee], all victims were reported to
have eaten beef or beef products in the last 10 years, but none had
knowingly eaten brain material. Furthermore, Stanley Prusiner, the scientist
who won the Nobel Prize in Medicine for his discovery of prions, describes
the levels of prions in muscle as "quite high." Follow-up studies in
Germany, published May 2003, confirm Prusiner's findings, and in 2003, the
New England Journal of Medicine published research indicating that deadly
prions were found in eight of the 32 muscle samples of human CJD victims.
The authors declare that the prions were "prevalent in skeletal muscle
tissue."

V. Final points: Watching abused farmed animals on TV and seeing pictures in
the news turns people vegetarian (as much out of empathy for the animals as
out of fear of getting the disease).

A. Mad cow disease opens a window onto the complete and total disdain that
factory farms have for the needs and natural lives of animals raised for
food. Modern "farmers" pump animals full of drugs to make them grow more
quickly, feed natural herbivores the blood and dead bodies of their own
species, and cram animals into unnatural living conditions where they are
deprived of their every natural desire. Animals today are Frankenstein
animals: Chickens are bred so that their upper bodies grow more than six
times as quickly as they normally would, and some cows produce as much as 20
times as much milk as they would in a natural situation. On factory farms,
animals' bodies are mutilated without painkillers. At a fraction of their
natural life spans, they are shipped to slaughter. The journey often takes
many hours, and on the way, animals endure weather extremes and are denied
food and water. Once they reach the slaughterhouse, many are fully conscious
as their throats are slit, their limbs are hacked off, and their skin is
ripped from their bodies. Before mad cow disease and foot-and-mouth disease,
most people had not thought very much about how meat reached their tables,
but these plagues forced people to think about these issues and made many
consider vegetarianism.

B. The public needs to understand that if they are eating meat in the USA, they are
supporting cruelty to animals-cruelty so severe that if it were done to cats
or dogs, it would be illegal, and these "farmers," truck drivers, and
slaughterhouse owners would be thrown in prison for cruelty to animals.
Outbreaks of diseases such as mad cow and foot-and-mouth disease are the
predictable results of treating animals like dirt, rather than like the
sensitive beings that they are.

I'm done with you. I'm not going to respond to your personal rants anymore. You should read your own article before posting:

Other than Charlene, a 24 year old woman now so tragically dying in Florida, who was probably infected in Britain, there have been no reported cases of variant CJD in the U.S.[14]

Dear Mr. Mc Candles; you reproach me for being a bad debater. I might be a bad debater , but I am certainly not an "early quitter" like you, just now it becomes interesting...

Can you read Mr. Mc Candles? When you quote me, please quote the whole paragraph please!

Other than Charlene, a 24 year old woman now so tragically dying in Florida, who was probably infected in Britain, there have been no reported cases of variant CJD in the U.S.[14] Hundreds of confirmed cases of the sporadic form of Creutzfeldt-Jakob disease, however, arise in the United States every year,[15] but the beef industry is quick to point out these are cases of sporadic CJD, not the new variant known to be caused by Mad Cow disease.[16] Of course, no one knows what causes sporadic CJD. New research, discussed below, suggests that not hundreds but thousands of Americans die of sporadic CJD every year, and that some of these CJD deaths may be caused by eating infected meat after all.

.

Think what you want, I addressed your comments with facts. You came back with nothing.

What facts from you are you exactly referring to Mr. McCandles? The one who comes with the real facts is me. I proved that eating pig brains is not 100% safe.

And now I will quote you;

Ok, since I proved that your disease is not an issue in our country, you are now attempting to change your original argument?

On the contrary; It was me again who proved that it is a major problem for thousands of Americans.
And about changing your mind; what about yourself Mr. McCandles? After reading the above, are you still persisting in your statement that the supplement you are reselling is 100% risk free for your customers?

Because obviously you do not have the balls to finish this with me; I will finish this conversation with quoting myself and a final thought;

First of all let me make one thing clear; I have nothing against you personally; You have a great website; nice layout, you are reselling also good stuff, against reasonable prices. But you are also reselling products that might cause potential health risks in human beings, and that bothers me.

Hopefully Eref could make a sticky from this topic as well, so customers could carefully select what is good and what is bad, and think twice when they are ordering something from you. Because I proved them it is definately not ALWAYS safe, and you might get terribly ill from some of your products. And you have clearly clarified yourself to us; you are only the reseller; if there are complaints; don't blame you; blame the manufacturer of the product! You are simply reselling anything, if you could earn money with it. No matter if the product could be potentially dangerous for human well being!

Speaking about moral and integrity Mr. McCandles; does that ring a bell?


To all; "Life is something valuable; don't gamble with it."

Sincerely yours,
Raymond Han

Raymond:

I'm sorry but you're really starting write like a real Don Qichote.

According to what you post, we have to boycot the whole meat industrie and allmost 50% of the supplements brought on the market these days.

Expecially while knowing the fact that Pigs, chickens, turkeys, and fish are not tested at all.

My god it's just what ErEf said earlier, we have become vegetarians soon.&o

Expecially while knowing the fact that Pigs, chickens, turkeys, and fish are not tested at all.

My god it's just what ErEf said earlier, we have become vegetarians soon.&o

Agreed, really sad

Well you can safely eat European bred animals now. Or, if you want to be absolutely sure, organically bred animals.

Remember.. the reason why mankind has developed the brains we have nowadays, is because we developed the ability to use tools to smash skulls and bones and pick out the precious DHA-fatty acids that we possess in more abundance than any other mammal on earth.
Nevertheless... in those days vegetarian species were never fed ground bones from other animals.. this is really sad!

Espi (glad I don't need to smash skulls anymore but rather can eat fish oil to get the valued DHA (and EPA) fatty acids)

secrete one word ook in nederlandse online suplementen winkels verkocht!

@espi;
@Barman;

Eating meat in the USA is not so safe as it is in the EU now;

1) To my understanding; Our Department of Agriculture banned the human consumption of cow brains, skulls, spinal cords, vertebral columns, eyes, and nerve tissue from cows older than 30 months.

2)In the EU Downer cows may no longer be eaten by humans. 'Downers' is the American term for cows which fall down and cannot stand up again because of sickness. In the USA they are still allowed to be boiled down and fed to chickens and pigs, and younger cow brains may still be eaten in the USA. These 'downer' cows may be infected with a type of BSE. And in America, the land of beef- and burger-eaters, there are 100 million cattle of which 300,000 die due to unexplained causes every year. It is really disgusting this is still allowed there!!!

3) European scientists recognize that TSEs can jump between species, and
thus, OUR countries have banned the feeding of animals to animals, but in
the U.S., it remains a legal and universal practice to feed pigs, chickens,
turkey, and fish back to one another, turning natural herbivores into not
just carnivores, but cannibals. Dr. Paul Brown, medical director for the
U.S. Public Health Service, explicitly says that pigs and chickens could
pass TSEs to humans. So beware of meat when you visit USA.

4)It is also illegal in the EU to feed ruminants (i.e., elk, deer, cows,
and sheep) to pigs, chickens, turkeys, and fish and then to feed those
animals back to cows and sheep, who are natural herbivores. Since they know
that sheep, deer, and elk in the U.S. have TSEs, they know that they are
continuing to do exactly what caused this disease in the first place. In the USA this is legal and "normal".

5)To avoid transmitting mad cow disease to humans, it is illegal in the
EU to feed any animal who is older than 30 months to humans. In
the U.S., on the other hand, almost all dairy cows, who are the source of
about 40 percent of U.S. hamburger meat, are older than 30 months of age
when they are slaughtered. So don't eat hamburgers in the USA, hamburgers in the EU are safer.

Maybe soulreavers father could confirm the above mentioned.

@Barman; Yes Secretagogue-1 is sold in European shops; that is exactly my point; these supplements contain anterior pituitary substance (vertaling; dierlijke hypofyses) from american cows or pigs; and because US regulations are not so strictly as ours; using these supplements are like a game of Russian Roulette.
Soon I am trying to get this supplement LAB tested in the Netherlands if it contains prions. According to MHP; source was pigs; as already stated before also pigs could be contaminated with PSE (Porcine Spongiform Encephalopathy) and could transfer it to human beings. Further investigation should prove this supplement is really safe. As for know; hands off!

Five diseases affect humans

There are five prion diseases known to affect humans - CJD, Gerstmann-Straussler-Scheinker disease, kuru, nvCJD, and fatal insomnia (slapeloosheid).

[image]local://upfiles/2748/0EB100EE835445028FD3664BFA6F5480.jpg[/image]Prion diseases damage the brain

They were originally - and are also - known as "transmissible spongiform encephalopathies" - transmissible because they can be transmitted between humans and animals, and spongiform encephalopathies because they often leave the brain riddled with holes like a sponge.

Creutzfeldt and Jakob were the first to discover such a disease. They described the disorder that bears their names between 1920 and 1921.

It first appeared as dementia, and progressed rapidly to destroy brain tissue and cause death.

What are the symptoms of Creutzfeldt Jacobs disease?

Creutzfeldt-Jakob disease displays striking similarities to kuru in regards to symptoms displayed and organ damage (mostly to the brain). Comparisons and parallels are evident between these two prion diseases. By inspecting an in depth case study of CJD from Massachusetts General Hospital, it is possible to gain a more complete understanding of prion diseases.

At age 47, a woman feeling depression sought professional help at Massachusetts General Hospital (Scully et al., 1993). She became hypoactive, noticed impairment of her recent memory, and had urinary incontinence (Scully et al., 1993). Within a few months she became dizzy and had an unstable gait (Scully et al., 1993). At this point a computed tomographic scan (CAT scan) of the brain showed slight cerebral and central atrophy; delusion began to set in (Scully et al., 1993). According to Scully et al. (1993), by age 50 the patient’s cranial-nerve functions were still normal, as well as motor power, sensation, and coordination. The next symptom to appear was the occurrence of inappropriate laughter, and her replies to questions became irrelevant and incorrect (Scully et al., 1993). Mild tremor was noted, although the cranial-nerve functions, strength, coordination, and sensation were still intact (Scully et al., 1993). At this time another CAT scan was performed, and the results were the same as the year before (Scully et al., 1993). Within a week after this scan, she was readmitted with shaking spells (Scully et al., 1993). There was a constant alteration between laughing and crying, but reflexes were still normal (Scully et al., 1993). By the age of 51 and a half years, her speech had deteriorated rapidly, and a new CAT scan showed marked cerebral and cerebellar atrophy (Scully et al., 1993). According to Scully et al. (1993), gradual deterioration continued up until her death four months prior to her fifty-fourth birthday.

Important similarities occur between Creutzfeldt-Jakob disease (CJD) and kuru. Both prion diseases cause tremor and inappropriate laughter. Depression was expressed early in CJD and in stage two of kuru. Unsteadiness in gait and sporadic muscle jerks were observed in both ailments. Dysarthria occurred in kuru during the initial stages of the diseases and in CJD more towards the end, and the exact same situation is seen with the condition of urinary incontinence as well.

[image]local://upfiles/2748/A75906DDAE0F4EB7865159E1E4BD15F0.gif[/image]
The effects of kuru include congestion of blood vessels, seen here, and in long-standing cases, cortical atrophy, not obvious here.

Attached Image(s)

Insecticides Cause Mad Cow Disease

Pharmaceutical interests in the UK are ignoring new scientific research that shows the insecticide used in the UK government's own warble-fly campaigns triggered the UK surge of 'Mad Cow' disease.

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

British scientists have led the current theory that an infectious prion in bonemeal fed to cattle causes bovine spongiform disease (BSE). Infectious prions are also claimed to cause new variant Creutzfeld-Jakob Disease (CJD) in humans -from ingesting beef. But the infectious prion theory serves to obscure a tragic chemical poisoning scandal behind the majority of BSE cases.

The new work proves that the prions can bond with manganese in animal feeds or mineral licks. These manganese prions cause the neurological degeneration seen in BSE. By a similar process, prions in human brains are damaged by lice lotions containing organophosphate. This can result in neurological diseases like CJD and Alzheimer's -later in life.

Many might be surprised to hear that organophosphates were developed by Nazi chemists during the course World War Two, as a chemical weapon nerve agent.

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


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

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

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

In the United States, the Environmental Protection Agency is already reviewing Phosmet's safety. The Centers for Disease Control in the US has recently conducted experiments on mice that confirm the organophosphate risk.

Not only is the EC beef slaughter campaign futile -because BSE disease is mostly noninfectious, but unless the underlying chemical cause is addressed, BSE will simply reappear from chemical causes. A new warble fly campaign is already underway in France using the organophosphate insecticide.

Of greater concern is that some lotions for scabies and head lice are now priming children and adults, for CJD and Alzheimer's in later life.
Bonding the Prion

Cambridge University prion biochemist, David R. Brown is dismissive of the science behind the infectious model of BSE. He terms it "a very limited amount of science by a few assumed- reputable scientists." He insists there is "no evidence an infectious agent is present in either meat or milk."

"Simple tests on udder walls of cows -- which could easily detect an infectious prion -- have not been done, why I don't understand."

A number of researchers have found that organophosphate(OP) in systemic warble fly insecticide can deform the prion molecule, rendering it ineffective at buffering free radical effects in the body. Worse still, the prion is then partial to bond with manganese and become a 'rogue' prion. A chain reaction whereby rogue prions turn others to rogues also, can explain the bovine spongiform disease mechanism.

Brown showed how prion protein bonds benignly with copper, but lethally with manganese. Even natural variations in relative environmental availability of manganese versus copper can trigger prion degradation.

The CJD and BSE symptoms mirror 'manganese madness', an irreversible fatal neuro-psychiatric degenerative syndrome that plagued manganese miners in the first half of the last century

Shining A Light On Spongiform

Organic dairy farmer and peer-review-published independent scientist, Mark Purdey, says the accepted theory of transmission from BSE-infected cattle to human CJD -by bonemeal or meat, is dependent on a mutant prion that has never been isolated under the scientific protocol called Koch's postulates.

Purdey's insistence on sticking to the letter of this scientific law earned him the condemnation of UK officialdom when he first mooted his theory. But Purdey pointed to CJD clusters downwind of a British Phosmet production plant to back his case.

He gave evidence to the UK Government BSE inquiry and was supported by Conservative MP, Thessa Gorman. His views were discounted, but his subsequent research and the new Cambridge prion work have confirmed the alternative theory. Despite this, and the backing of a British peer, he is denied even exploratory funding.

Why does CJD degeneration in humans begin in the retina, and why are CJD disease clusters found in high altitude locations?

The prion molecule has a known natural role as a shock absorber of damaging energy from ultraviolet rays and other oxidizing agents.

Once this prion defense system is rendered ineffective by organophosphates - for example in human head lice lotions, these oxidizing effects have an unmediated impact on tissues. Eventually, UV radiation damages the retina and oxidative stress destroys the brain tissues of CJD patients. This theory would expect to find higher CJD incidence in mountain regions -where UV radiation levels are elevated. That prediction holds true.

A similar but accelerated mechanism could be driving BSE. ICI's Phosmet organophosphate warble fly insecticide -applied on the backs of animals along the spinal column, similarly degrades prions. "Systemic versions of the insecticide are designed to make the entire cow carcass toxic to warble fly," explains Purdey. "Unfortunately it's toxic to prions too -especially those prions located just millimeters from the point of application."

The damaged prions are then ready to react with manganese in animal feed, or manganese sprayed on land or in mineral licks -to become the driving force of BSE neurodegeneration. Purdey says manganese-tipped prions set off lethal chain reactions that neurologically burn through the animal.

Chickens notoriously excrete most of the supplements fed to them -including manganese. And their manganese-rich excreta have been blended into cattle feed in the UK. Natural variations in the relative environmental availability of copper and manganese can also spur prion degeneration says Purdey.

From this research, any prudent person would conclude there is a significant risk attaching to the use of organophosphate in humans. Preparations for head lice and scabies are known to be overused in practice and might be priming users for CJ disease.

The Money Trail

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

There are more explosive implications to his -and other's latest research. Purdey says similar organophosphate-induced protein deformation could also underlie Alzheimer's disease. If that were true, the litigation fallout would destroy some pharmaceutical giants, and a lot of very influential noses would be out of joint.

Disturbingly, Purdey and other brain researchers seem to have had an undue share of unfortunate accidents. Purdey's house was burned down and his lawyer who was working with him on Mad Cow Disease was driven off the road by another vehicle and subsequently died. The veterinarian on the case also died in a car crash -locally reported as: 'Mystery Vet Death Riddle.'

Dr. C. Bruton, a CJD specialist -- who had just produced a paper on a new strain of CJD -- was killed in a car crash before his work was announced to the public. Purdey speculates that Bruton might have known more than what was revealed in his last scientific paper.

In 1996, leading Alzheimer's researcher Tsunao Saitoh, 46 and his 13 -year-old daughter were killed in La Jolla, California, in what a Reuters report described as a "very professionally done" shooting.

EIONews.com December, 13 2000

[image]local://upfiles/2748/B60C287B92D54151860A7FC78A5315F8.jpg[/image]
How BSE is triggered by OP Insecticide and Manganese

[image]local://upfiles/2748/63B2F9F28E6B4BC8912F88D33B8F9622.jpg[/image]
Chickens notoriously excrete most of the supplements fed to them -including manganese

Read it yourselves here; http://www.eionews.addr.com/organop/organop.htm
and Purdey's website; http://www.purdeyenvironment.com/

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ORIGINAL: Esperantistino

Well you can safely eat European bred animals now. Or, if you want to be absolutely sure, organically bred animals.

I do really hope so Espi; but what really bothers me is that soulreavers dad is not allowed to confirm this.
I am wondering if it is still allowed in the EU to boil down "downer cows" and feed this back to one another, or even feed it to sheep, pigs, chicken, causing scrapie (TSE in sheep) and PSE (Porcine Spongiform Encephalopathy) in pigs. Downer cows are cows who are too sick to stand on their legs and fall down. Carcasses of these cows could be infected whith BSE. In this case prions return in the food chain. As far as I know it is not allowed anymore, so a confirmation from Soulreaver's dad could put everybodies mind at ease (at least in the EU). Also it would be fine to know if the EU imports much meat from USA, where this is "normal".

Because of the long incubation time (10-30 years) people do not notice they are infected with prions, because the immune system does not detect this. Once infected by prions people could get Alzheimer and CFJ disease on a later state in life. (But then it is generally accepted that old people start loosing their memory; and nobody will make the connection with contaminated meat anymore). This is really scary!!
I am wondering if these infected people could transfer the disease to other human beings via blood transfusions? Maybe Soulreavers dad could confirm this is really impossible (hopefully).

Also I am curious to know what the restrictions are in the EU to use ICI's Phosmet organophosphate warble fly insecticide -applied on the backs of animals along the spinal column, similarly degrading prions. Systemic versions of the insecticide are designed to make the entire cow carcass toxic to warble fly, which could ultimately trigger BSE in cows.