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Does cooking protect meat?
- Thread starter -ooO-(GoldTrade
- Start date
For the veggie lover ( I actually love both)
1. Were your favorite veggies organically grown? (fertilized with manure from BSE cows or peed on by wild deer with the same condition, or fertilized with bone meal, and other tankage products from rendered sick animals)(next time you are in the gardening section read the label on the rose fertilizer, think that is the only place it is used, think again)
2. Were your veggies grown inorganically? (treated with phosphate fertilizers, pesticides, herbicides, and fungicides)
3. Were they domestically grown? (which US haters don't trust)
4. Were they imported? ( no known history or inspection procedures, no history of chemical treatment of cleanliness handling procedures)
If you think there is a foolproof absolutely safe route you are in delusion. Just look around and see who is sickened and dying of what and then relax about our food supply.
1. Were your favorite veggies organically grown? (fertilized with manure from BSE cows or peed on by wild deer with the same condition, or fertilized with bone meal, and other tankage products from rendered sick animals)(next time you are in the gardening section read the label on the rose fertilizer, think that is the only place it is used, think again)
2. Were your veggies grown inorganically? (treated with phosphate fertilizers, pesticides, herbicides, and fungicides)
3. Were they domestically grown? (which US haters don't trust)
4. Were they imported? ( no known history or inspection procedures, no history of chemical treatment of cleanliness handling procedures)
If you think there is a foolproof absolutely safe route you are in delusion. Just look around and see who is sickened and dying of what and then relax about our food supply.
Check out the fda.gov and cdc.gov explanations of BSE and vCJD. You can find a link to the official info on Mad Cow Disease on the front page of both sites. Their explanations aren't tainted with vegan propaganda, though they are of course too cautious so as to avoid creating widespread panic.
As for proof--nobody really has any scientifically rigorous proof of a connection between prions and BSE and vCJD, just "strong scientific evidence." We really don't know enough about the diseases yet to say for sure...
As for proof--nobody really has any scientifically rigorous proof of a connection between prions and BSE and vCJD, just "strong scientific evidence." We really don't know enough about the diseases yet to say for sure...
__________________________________________Quote from dchang0:
Check out the fda.gov and cdc.gov explanations of BSE and vCJD. You can find a link to the official info on Mad Cow Disease on the front page of both sites. Their explanations aren't tainted with vegan propaganda, though they are of course too cautious so as to avoid creating widespread panic.
As for proof--nobody really has any scientifically rigorous proof of a connection between prions and BSE and vCJD, just "strong scientific evidence." We really don't know enough about the diseases yet to say for sure...
Exactly! No proof just evidence that prions cause BSE and or vCJD but that is only in their own specific species. Absolutely no evidence that prions in bovines cause prions in humans or transfer to humans since they are different prions to begin with.
The same with scrapie in sheep and CJD in wild deer all maybe caused by prions unique to each species.
Do people get cancer? So do the other 3 species but is cancer contagious?
Check the per capita consumption figures for beef since the BSE scare there in May. Guess what they have gone up! Maybe common sense prevails after all.
Bovine Spongiform Encephalopathy or âMad Cow Diseaseâ and New Variant Creutzfeldt-Jakob Disease
The issue of whether there is a direct link between the exposure to diseased animals and the acquisition of CJD has been the subject of much scientific study and debate. In the United Kingdom, scientists have ascertained a likely connection between bovine spongiform encephalopathy ("BSE") and CJD. BSE or "mad cow disease" was initially discovered in the United Kingdom in 1986 and thought to have resulted from the use of cattle feed containing contaminated meat and bone meal made from scrapie-infected sheep and/or TSE-infected cattle. The original outbreak was then probably magnified by subsequently feeding meat and bone meal from BSE-infected cows to young calves. The incidence of BSE in the United Kingdom reached its peak of over 36,000 confirmed cases in one year in 1992, and has been steadily declining. There have been over 180,000 BSE cases worldwide, with the overwhelming majority, over 95%, occurring in the United Kingdom. The other countries in which BSE has been found include: Austria, Belgium, Czech Republic, Denmark, Finland, France, Germany, Greece, Ireland, Israel, Italy, Japan, Luxembourg, Liechtenstein, the Netherlands, Poland, Portugal, Slovakia, Slovenia, Spain, and Switzerland. The number of BSE cases in countries outside of the United Kingdom is increasing. BSE has not been detected in the United States.
On March 20, 1996, the United Kingdomâs Spongiform Encephalopathy Advisory Commmitte (âSEACâ) indicated that there was a possible link between BSE and a new variant of CJD (âvCJDâ). The SEAC identified 10 patients, whose illness surfaced in 1994 and 1995, with a form of CJD which differed significantly from classical sporadic CJD in several respects. These ten patients were all under the age of 42, with an average age of 28, as opposed to the typical age of 63 for classical CJD. The average course of the duration of vCJD was 13 months, in contrast to the average 4 to 6 month duration for classical CJD. The electroencephalographic (âEEGâ) electrical activity in the brain for vCJD was different from classical CJD. While the brain pathology of the vCJD cases was identifiable as CJD, the pattern differed from classical CJD with the presence of large aggregates of prion protein plaques. Despite the absence of direct scientific evidence linking BSE and vCJD, the SEAC decided that the most likely explanation for the unusual outbreak was the consumption of beef from diseased cattle before 1989, when regulations were adopted for the disposal at slaughter of potentially infectious cattle offal, including brains, spinal cords and intestines, and for the cessation of feeding protein derived from ruminants (i.e. cows, sheep, goats, deer and elk) to ruminants. Subsequent studies have strengthened the connection between BSE and vCJD.
There have been over 100 cases of vCJD, most of which have occurred in the United Kingdom, and the numbers are still rising. A few cases of vCJD have been found in France, Ireland, Italy, and Hong Kong. Because the incubation period between exposure to the TSE agent and the onset of symptoms may be as long as 40 years, it is uncertain whether these vCJD cases may signal the beginning of an epidemic or whether the incidence of vCJD will remain low. At the present time, no vCJD has been discovered in the United States.
:eek:
The issue of whether there is a direct link between the exposure to diseased animals and the acquisition of CJD has been the subject of much scientific study and debate. In the United Kingdom, scientists have ascertained a likely connection between bovine spongiform encephalopathy ("BSE") and CJD. BSE or "mad cow disease" was initially discovered in the United Kingdom in 1986 and thought to have resulted from the use of cattle feed containing contaminated meat and bone meal made from scrapie-infected sheep and/or TSE-infected cattle. The original outbreak was then probably magnified by subsequently feeding meat and bone meal from BSE-infected cows to young calves. The incidence of BSE in the United Kingdom reached its peak of over 36,000 confirmed cases in one year in 1992, and has been steadily declining. There have been over 180,000 BSE cases worldwide, with the overwhelming majority, over 95%, occurring in the United Kingdom. The other countries in which BSE has been found include: Austria, Belgium, Czech Republic, Denmark, Finland, France, Germany, Greece, Ireland, Israel, Italy, Japan, Luxembourg, Liechtenstein, the Netherlands, Poland, Portugal, Slovakia, Slovenia, Spain, and Switzerland. The number of BSE cases in countries outside of the United Kingdom is increasing. BSE has not been detected in the United States.
On March 20, 1996, the United Kingdomâs Spongiform Encephalopathy Advisory Commmitte (âSEACâ) indicated that there was a possible link between BSE and a new variant of CJD (âvCJDâ). The SEAC identified 10 patients, whose illness surfaced in 1994 and 1995, with a form of CJD which differed significantly from classical sporadic CJD in several respects. These ten patients were all under the age of 42, with an average age of 28, as opposed to the typical age of 63 for classical CJD. The average course of the duration of vCJD was 13 months, in contrast to the average 4 to 6 month duration for classical CJD. The electroencephalographic (âEEGâ) electrical activity in the brain for vCJD was different from classical CJD. While the brain pathology of the vCJD cases was identifiable as CJD, the pattern differed from classical CJD with the presence of large aggregates of prion protein plaques. Despite the absence of direct scientific evidence linking BSE and vCJD, the SEAC decided that the most likely explanation for the unusual outbreak was the consumption of beef from diseased cattle before 1989, when regulations were adopted for the disposal at slaughter of potentially infectious cattle offal, including brains, spinal cords and intestines, and for the cessation of feeding protein derived from ruminants (i.e. cows, sheep, goats, deer and elk) to ruminants. Subsequent studies have strengthened the connection between BSE and vCJD.
There have been over 100 cases of vCJD, most of which have occurred in the United Kingdom, and the numbers are still rising. A few cases of vCJD have been found in France, Ireland, Italy, and Hong Kong. Because the incubation period between exposure to the TSE agent and the onset of symptoms may be as long as 40 years, it is uncertain whether these vCJD cases may signal the beginning of an epidemic or whether the incidence of vCJD will remain low. At the present time, no vCJD has been discovered in the United States.
:eek:
What Are The Symptoms of Creutzfeldt-Jakob Disease?
There are several common symptoms evident in CJD patients as the disease runs its course. The average duration of CJD from the onset of symptoms to the inevitable death is four to six months. Most patients die within one year; however, longer duration periods of two or more years have been noted, usually in the familial form and with an earlier age of onset.
The initial stage of the disease can be subtle with ambiguous symptoms of insomnia, depression, confusion, personality and behavioral changes, strange physical sensations, and problems with memory, coordination and sight. As the disease advances, the patient experiences a rapidly, progressive dementia and in most cases, involuntary and irregular jerking movements known as myoclonus. Problems with language, sight, muscular weakness, and coordination worsen. The patient may appear startled and become rigid. In the final stage of the disease, the patient loses all mental and physical functions. The patient may lapse into a coma and usually dies from an infection like pneumonia precipitated by the bedridden, unconscious state.
:eek:
There are several common symptoms evident in CJD patients as the disease runs its course. The average duration of CJD from the onset of symptoms to the inevitable death is four to six months. Most patients die within one year; however, longer duration periods of two or more years have been noted, usually in the familial form and with an earlier age of onset.
The initial stage of the disease can be subtle with ambiguous symptoms of insomnia, depression, confusion, personality and behavioral changes, strange physical sensations, and problems with memory, coordination and sight. As the disease advances, the patient experiences a rapidly, progressive dementia and in most cases, involuntary and irregular jerking movements known as myoclonus. Problems with language, sight, muscular weakness, and coordination worsen. The patient may appear startled and become rigid. In the final stage of the disease, the patient loses all mental and physical functions. The patient may lapse into a coma and usually dies from an infection like pneumonia precipitated by the bedridden, unconscious state.
:eek:
http://www.cultureshop.org/details.php?code=PURDEY
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techstaion-
In light of British panic over mad cow, their Spongiform Encephalopathy Advisory Committee has been closely studying and monitoring these diseases since 1990. On March 20, 1996 it noted 10 cases of human CJD that occurred in younger people and lasted longer than typically seen. Besides the fact that most variant-CJD victims had eaten beef at some time -- although no one had eaten brain tissue and one of the ten patients had been a vegetarian since 1991 -- they could find no scientific evidence linking BSE and vCJD.
That didn't stop vCJD from being labeled the human form of mad cow. A popular orthodoxy has evolved, fueled by media frenzy, that meat contaminated with the brain prions of mad cows could give people the disease. "It's all been much ado about nothing," said Scott C. Ratzan, director of the Emerson College/Tufts University School of Medicine Program in Health Communications and editor of the Journal of Health Communications. "Based on available scientific evidence, we can be virtually certain that mad cow disease poses no threat to humans."
While several studies published in Nature reported an association between vCJD and BSE, they are far from conclusive and other researchers question the theory. No one has ever been able to establish that any vCJD victim has ever eaten beef from a diseased animal or that infected prions can cross the species barrier and cause disease in humans. There also aren't increased cases in cultures where brains are a favorite dish. Transmission from other exposures doesn't hold up, either, as there's no higher incidence among farmers, slaughterhouse workers, butchers or others in greater contact with BSE or animal products.
__________________________________________
___________________________________________
techstaion-
In light of British panic over mad cow, their Spongiform Encephalopathy Advisory Committee has been closely studying and monitoring these diseases since 1990. On March 20, 1996 it noted 10 cases of human CJD that occurred in younger people and lasted longer than typically seen. Besides the fact that most variant-CJD victims had eaten beef at some time -- although no one had eaten brain tissue and one of the ten patients had been a vegetarian since 1991 -- they could find no scientific evidence linking BSE and vCJD.
That didn't stop vCJD from being labeled the human form of mad cow. A popular orthodoxy has evolved, fueled by media frenzy, that meat contaminated with the brain prions of mad cows could give people the disease. "It's all been much ado about nothing," said Scott C. Ratzan, director of the Emerson College/Tufts University School of Medicine Program in Health Communications and editor of the Journal of Health Communications. "Based on available scientific evidence, we can be virtually certain that mad cow disease poses no threat to humans."
While several studies published in Nature reported an association between vCJD and BSE, they are far from conclusive and other researchers question the theory. No one has ever been able to establish that any vCJD victim has ever eaten beef from a diseased animal or that infected prions can cross the species barrier and cause disease in humans. There also aren't increased cases in cultures where brains are a favorite dish. Transmission from other exposures doesn't hold up, either, as there's no higher incidence among farmers, slaughterhouse workers, butchers or others in greater contact with BSE or animal products.
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Quote from Doubter:
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I agree with you totally but I believe what the 120 people worldwide have is vCJD not BSE. It is a human similar condition but what I am asking is proof that one causes the other and as far as I can tell there is no known connection.
My grandmother died in 1994 of CJD. After her autopsy it was verified as one of the first cases in the U.S. since then my family has been very active in the "CJD voice" and other support groups. Dr Stanley Prusiner himself verified her death was from CJD(if you don't know the name do a YHOO search). I am telling you guys and gals who do not want to believe it that the numbers are much greater than the "1 in a million stats" the gov has released. And the part about it not being genetically passed on has not been proven false. MY MOTHERS COUSINS MOTHER ALSO DIED FROM IT!!!. I CAN PROVE ALL OF THIS IF ANYBODY IS SO INCLINED TO TALK VIA E-MAIL. My whole family is not allowed to give blood, donate organs or bone marrow....it is very scary.