EU ruling raises the spectre of 'mad cow disease'
Lifting a ban on feeding meat to animals could raise the spectre of "mad cow disease" and hit public confidence in the safety of British beef.
The European Commission (EC) is considering easing rules introduced to combat the spread of BSE 20 years ago to allow feed containing animal proteins.
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Neil Parish
It wants to reduce the cost of guarding against the disease, Bovine spongiform encephalopathy, and its human form, Creutzfeldt Jacob Disease (CJD), which has claimed 169 British lives since 1995.
In a consultation document, the Commission claimed the changes would be based on sound science and would reduce farmers' dependency on crop-based alternatives and their volatile foreign markets.
But the report admitted it was "impossible" to remove all risk of the disease entering the food chain. Bridgwater farmer Neil Parish, the Conservative MP for Tiverton and Honiton and a former EU agriculture committee chairman, said the public needed reassurance that there was no contamination of the meat and bone meal feed.
"What was so wrong before was that we were feeding meal back to the same species," said Mr Parish, who is also a dairy farmer.
John Hore, NFU South West regional livestock board chairman, who farms in South Gloucestershire, said provided consumer safety was paramount and any change was backed by science, he was comfortable with a gradual unravelling of the legislation introduced in the wake of the BSE crisis.
He said: "The absolute key to this is consumer safety. The big no-no is obviously intra-species recycling. But the red tape has a huge cost and if the controls can be gradually unravelled, where safe, I think it's the right thing to do."
The key animal health control for BSE is the ban on feeding meat and bone meal produced from ruminants (cattle, sheep and goats) back to the same species. Since the first case of BSE was discovered in 1986, 181,114 cattle have been diagnosed with the disease and four million culled. The condition was sparked by cattle eating animal feed containing infected proteins from a sheep which had died of a related disease, scrapie.
At the height of the health and political crisis, the issue dominated the headlines and the then government tried to play down public health fears. This led to the decision of then cabinet minister John Selwyn Gummer to publicly feed his four-year-old daughter Cordelia a burger to prove beef was safe. But in recent years there has been a sharp decline in reported cases in cattle, with numbers between 2007 and 2009 falling from 53 to nine.
The EC is awaiting new scientific evidence on allowing a "tolerable" level of animal proteins in feed from the European Food Safety Authority. The National Farmers' Union said that with almost a third of UK livestock raised in the South West, regional concerns were understandable. Spokesman Ian Johnson said: "Farmers just want to know that nobody is going to be put off their product – so much was shrouded in secrecy before and we don't want to go back to those days."
The Government says it is concerned about tolerance levels for processed animal protein, except fishmeal, in ruminant feed as this could risk feeding ruminant meat and bone to ruminants.
Gillian Turner, of the CJD Support Group, said the "science just isn't there" and urged the EU to be cautious.







10 Comments
by hlasnych, Czech Republic
Monday, September 13 2010, 10:49PM
“May eyes of cattle become new windows to detect mad cow disease?
A team of researchers, led by Iowa State University, US, says that the eyes of cattle may reveal signs of neurological disorders such as mad cow disease. The team examined the retinas of sheep infected with scrapie - a disease similar to BSE, or mad cow disease. They found that the retinas of infected sheep emitted a characteristic "glow". The study appears in the journal Analytical Chemistry ( http://esciencenews.com/articles/2010/09/08/eyes.cattle.may.become.new.windows.detect.mad.cow.disease).
Most cases of BSE in Great Britain have occurred in dairy cows between 3 and 6 years of age. Cows affected by BSE show a reduced time spent ruminating, although eating time is maintained at normal levels. This reduction can be marked and rumination can cease (AUSTIN and SIMMONSON, 1993).
In the eye, the thin layer of tissue that lies between the sclera and the retina is the choroid. This is rich in blood vessels that nourish the retina, and the dark pigments of the choroid absorb light rays so that they are not reflected back out of the eye. STEINLE et al. (2000) concluded that sympathetic -noradrenergic vasoconstriction occurs throughout the choroid, whereas parasympathetic nitrergic vasodilation plays a selective role in modulating blood flow in anterior tissues of the eye. Choroidal blood flow in eyes is light driven and controlled by a parasympathetic input from ciliary ganglion (KIMBLE et al., 2006). In addition, CUTHBERTSON et al. (2003) about the retina parasympathetic control found that with the FG (fluorochrome) labeling is evident a strong white glow in the choroid and sclera. Now researchers found that the retinas of infected sheep emitted a distinct ¿glow¿; the scrapie-positive retinas fluoresce a lot - they gave a lot of light back, and this light was very structured....
So we can say that the loss of parasympatetic function can be found when the sympathetic nervous system (SNS) prevails and sympathetic vasoconstriction occurs throughout the choroid- in spongiform encephalopathies. And finally can we conclude; spongiform encephalopathies- as a loss of parasympathetic function ?
In addition, calcium and magnesium regulate the SNS which controls our "fight or flight" reaction. SNS is stimulated by calcium, and inhibited by magnesium. According to ¿BSE ammonia- magnesium ¿theory (www.bse-expert.cz), the origins of the diseases may lie in chronic magnesium deficiency (coupled with a high protein intake in ruminants).”
by hlasnych, Czech Republic
Monday, September 13 2010, 10:11AM
“BSE is more political than health orientated; see ¿Meat Trade News Daily¿(13 Sep 2010)
(http://www.meattradenewsdaily.co.uk/news/130910/neterlands___bse_is_more_political_than_health_orientated_.aspx);
A 10-year-old cow in the Netherlands has tested positive for BSE, more commonly known as "mad cow" disease, the first such result in more than two years.
Mad cow disease, bovine spongiform encephalopathy (BSE), first emerged in Britain in the 1980s and has been found in herds in several European and other countries. Scientists believe it is transmitted through infected meat and bone meal fed to cattle and it is thought to cause vCJD in humans.
Here are some key facts:
THE ORIGINS:
* The disease first surfaced in Britain in 1985 when a black-and-white dairy cow was seen staggering and head-butting other cattle. It was diagnosed as BSE in November 1986.
* Known formally as bovine spongiform encephalopathy, the disease swept through Britain in the 1980s and early 1990s, leading to millions of animals being slaughtered and burnt.
* Scientists blamed the disease's spread on waste produced in slaughterhouses and used to make animal feed. Cattle feed usually contained waste from the slaughter of other cows.
THE COST:
* Britain destroyed 3.7 million cattle in the 1980s and 1990s because of BSE. Between 1986 and 2002, 181,376 cases were confirmed in Britain.
-- During that time Britain spent more than $6 billion, excluding job losses, in sorting out the crisis.
* The worldwide ban on British beef exports imposed after the emergence of BSE in 1980s was partially lifted in 1999. In March 2006, EU experts agreed to a complete lifting of the embargo, nearly 10 years to the day after it was imposed....”
by hlasny, Bludov, Czech Republic
Saturday, September 11 2010, 7:06PM
“So about the BSE/ vCJD diseases; this was never justified scientifically. In 1996, a variant form of Creutzfeldt-Jakob disease (vCJD) was discovered in small clusters in Britain. It was immediately suspected that the outbreak of BSE could be connected to the clusters of vCJD in humans. Because of the 100%mortality rate of both diseases, the British government issued a "Mad Cow Warning." People were cautioned not to eat beef that may come from diseased cattle, for fear the disease could be transmitted to humans via the meat products they consumed.
However, WHY the number of vCJD cases peaked in 2000 and is now declining ? There are my responses; Over the next few years, researchers desperately searched for the cause of BSE and any possible connection to the human variant (vCJD). The first theory that appeared to make sense was that British cattle were being fed meat and bone meal (MBM) feed that included potentially contaminated brain and spinal cord matter that could the source of the disease in cows. Theoretically, eating contaminated meat could transfer the disease to the human population.
Upon further research, the connection to the human vCJD, was thought to exist because an abnormal prion protein (PrPsc) that was found in both diseased cattle and infected human brain and spinal cord cells. This abnormal prion protein causes the normal prion proteins to convert to abnormal prion proteins. Once enough prion proteins are converted, they cause the death of neurons (brain cells) in both cattle and humans.
Over a 14 year period, there were 115 confirmed cases of variant CJD that were closely examined. None of them could establish a clear connection to beef consumption. By this time, scientific theories had become fact in the minds of the general public. No additions, corrections or retractions to the previous information given to the public were printed by either the media, or government officials. There is still very little evidence to support the idea that BSE (mad cow disease) can be transmitted to humans by any means other than perhaps eating brain and spinal cord tissue (even that is not certain).
Several experts have continued to research BSE and vCJD trying to uncover causes and possible connections despite the lack of funding. Funding is extremely difficult to obtain because there is already an "acceptable theory" out there and no one seems to care whether it is accurate or not.
Some of the theories established by ongoing research. According to my theory, the origins of the diseases may lie in chronic magnesium deficiency coupled with a high protein intake. So defective prions are markers of the diseases rather than the cause and BSE can be a naturally occurring disease, not an infectious disease.”
by hlasny, Bludov, Czech Republic
Saturday, September 11 2010, 6:40PM
“Continued...
It is almost universally accepted that the normal protein (PrPc) is a metal binding protein. PrPc was first suggested to be a copper (Cu) binding protein in the early 1990¿s and confirmed by David Brown and colleagues in 1997 (BROWN,D.R., 2001). Recently the team of professor BROWN repeatedly pointed out that elevated manganese (Mn) was associated with prion infection - in field cases and experimentally infected animals (BSE and scrapie). So sheep infected with scrapie and cows infected with BSE have elevated levels of Mn in their tissues before clinical symptoms appear, according to new research. These findings were published by the Brown´s team in the Journal of Animal Science (HESKETH et al., 2007)
However, there could be a possibility; increased the Mn absorption and retention
can be found in the longer-term Mg deficiency. Mn2+ is very similar to Mg2+ in terms of its chemical properties, including inner and outer shell complexation. In biological systems, only Mn2+ is readily capable of replacing Mg2+, and only in a limited
set of circumstances. The body can replace Mn with Mg with similar efficiency in Mn-activated proteins (WAPNIR, 1990). Similarly, Mn can occupy Mg allosteric sites in Mg-activated proteins, such as the sarcoplasmic reticulum Ca- ATPase (CHIESI and INESI,1981). Mn2+ effectively binds ATP and allows hydrolysis of the energy molecule by most ATPases.
Investigated the relationship between Mg deficiency and Mn metabolism, YASUI et al
(1995) found that Mn content in central nervous system tissues and visceral organs was highest in rats fed a low Ca-Mg diet. SANCHEZ- MORITO et al. (1999) found that feeding rats a diet deficient in Mg decreased urinary and fecal Mn excretion. They also observed greater Mn retention in skeletal muscle, heart and kidney in Mg-deficient rats as compared to control. They concluded that under experimental conditions, Mg deficiency increased Mn absorption, which was reflected as increased Mn deposits in all soft and hard tissues studied except the sternum and liver
Some other of the BSE- alternative theories established by ongoing research. Also alternative ¿BSE ammonia- magnesium theory¿ is well known in the world from 2002 (http://www.agriworld.nl/feedmix/headlines.asp?issue=3), see the full text. ¿Lone voices in the BSE debate¿ (www.warmwell.com/lone_voices_in_the_bse_debate[...). According to this theory, the origins of the diseases may lie in chronic magnesium deficiency coupled with a high protein intake. So defective prions are markers of the diseases rather than the cause and BSE can be a naturally occurring disease, not an infectious disease. See also other relationships (WHY great progress about BSE eradicating within the EU...?) , according to my web www.bse-expert.cz and recent presentation at 29th World Veterinary Congress in Vancouver; Neurodegenerative Diseases and Schizophrenia as a Hyper or Hypofunction of the NMDA Receptors (www.bse-expert.cz/pdf/Veter_kongres.pdf). Described findings about "manganese theory" (Mark Purdey) act in concert with other eco-detective "BSE ammonia- magnesium theory" (Josef Hlasny).
So ¿infectious prions¿ found in normal brain tissue act in concert about; magnesium (Mg)deficiency and higher manganese (Mn) absorption- deposition ?”
by hlasny, Bludov, Czech Republic
Saturday, September 11 2010, 6:27PM
“Until recent time in the scientific literature we have read, seen, heard... ; scientists believe mad cow disease (BSE) spreads when farmers feed cattle recycled meat and bone meal (MBM) from infected animals. The disease is also believed to be linked to the rare but fatal human variant, Creutzfeldt-Jakob disease (vCJD).
But a few weeks ago, we were able to read; Infectious agents of the sort believed to cause mad cow disease in humans can appear ¿as if from nowhere¿ when healthy brain tissue comes into contact with steel when scientists observed several unexpected instances of infectious prions in control groups where metal wires had been exposed only to uninfected normal mouse brain tissue...
In a startling new study that involved research on both sides of the Atlantic, scientists from The Scripps Research Institute in Florida and the University College London (UCL) Institute of Neurology in England have shown for the first time that abnormal prions, bits of infectious protein devoid of DNA or RNA that can cause fatal neurodegenerative disease, can suddenly erupt from healthy brain tissue See the article published in PNAS- July 2010 (http://www.pnas.org/content/early/2010/07/16/1004036107).
They noted that an alternative interpretation of the results is that infectious prions are naturally present in the brain at levels not detectable by conventional methods, and are normally destroyed at the same rate they are created. If that is the case, they noted, metal surfaces could be acting to concentrate the infectious prions to the extent that they became measurable by the team's testing methods.
The catalyst used in their study was a simple steel wire (or stainless steel?). Steel is an alloy that consists mostly of iron and has a carbon content between 0.2% and 2.1% by weight, depending on the grade. Carbon is the most common alloying material for iron, but various other alloying elements are used, such as manganese (Mn)... Varying the amount of alloying elements and the form of their presence in the steel (solute elements, precipitated phase) controls qualities of the resulting steel
According to some researchers, the deformed prions would become more prone to binding with manganese (Mn), and it is this combination that makes them dangerous. It is postulated that Mn -bound prions then become rogue prions that have the ability to deform other normal prions in a chain reaction that eventually destroys the brain. This hypothesis contends that TSEs are likely linked to environmental conditions rather than prion-contaminated feed. The researchers discovered that prions require copper (Cu) to develop properly. If Cu is low and exposure to high levels of Mn occurs, the prion may bind to Mn and turn into the fatal form that eventually burns holes in the brain.
Continued...”
by Hazel, Somersetshire
Thursday, September 09 2010, 7:47PM
“What bright spark thought of that.No way should that be allowed to happen. As it should not have done before.I had no idea the cows were eating their mates.In the end their pee was very pink so that was a rush around I can tell you. Hi charles how be.
Toots 1939”
by Hazel, Wells
Thursday, September 09 2010, 4:49PM
“Good lord what a shock.The animals to eat each other again.No way.What bright spark thought of that.It should never have happened before,and should never happen again. My cows ended up peeing dark red. That was a rush around
I can tell you. Hi Charles how be.
Toots1939”
by hlasny, Bludov, Czech Republic
Wednesday, September 08 2010, 7:59PM
“You wrote; ¿the public needed reassurance that there was no contamination of the meat and bone meal feed¿.There are two dissenting or eco- detective voices; ¿mad cow disease¿ (BSE) can be a naturally occurring disease, so not an infectious disease, so beef is (was) safe in the all world. WHY? Because the connection about BSE/ vCJD diseases; this was never justified scientifically! It was pure, math-model-driven science fiction. But it was pushed very vigorously by the British science establishment, which has never confessed to its errors... See more about the; BSE/ vCJD mathematical- models, see my large comments in Telegraph.co.uk (www.telegraph.co.uk/health/healthnews/7168326/D oes-vCJD-still-pose-a-major-public-health-threat .html). See also other relationships (WHY great progress about BSE eradicating within the EU...?) , according to my web www.bse-expert.cz and recent presentation at 29th World Veterinary Congress in Vancouver; Neurodegenerative Diseases and Schizophrenia as a Hyper or Hypofunction of the NMDA Receptors (www.bse-expert.cz/pdf/Veter_kongres.pdf). So according to my theory the story of BSE in Britain is a consequence of ¿intensive farming" (metabolic disease disease and ¿neurotoxicity") and belongs in the ¿agricultural ecology"...
Also Mark Purdey (1953- 2006) organic dairy farmer in Somerset was a maverick figure in the study of one of the largest public-health scares of the last century. He became convinced that BSE had been caused not by feed containing scrapie-infected sheep offal, as was the received wisdom... Purdey set about studying several countries affected by TSEs and those where it was completely absent. His results appeared to suggest that a combination of high manganese levels, low copper levels... could bring about TSEs in susceptible genotypes. One of the implications of his theory was that fears of transmission were unfounded, and that thousands of cattle had been slaughtered unnecessarily. He spent many years, and many thousands of pounds, trying to convince the Government...”
by Charles Henry 1945-(diuturnity), Somersetshire
Wednesday, September 08 2010, 10:46AM
“:| What I want to know is just WHY and WHO is putting this forward again now?. Just what purpose is being is being served by any of this?. . Clearly the farming community, at the 'sharp end', don't want any part of it. . Just what are the EC playing at!? . Are they just trying to generate an anti-farming, anti-meat environment again with this now 'highly political disease'? . I don't believe they can't be trusted any further than we can throw them.”
by Charles Henry 1945-(diuturnity), Somersetshire
Wednesday, September 08 2010, 10:11AM
“:| What I want to know is just WHY and WHO is putting this forward again now. . Just what purpose is being is being served by any of this. . Clearly the farming community, at the 'sharp end', don't want any part of it. . Just what are the EC playing at!? . Are they just trying to generate an anti-farming, anti-meat environment again with this 'highly political disease'. . They can't be trusted any further than we can throw them.”