A Shropshire Euro MP says county farmers have been given a boost after the European Commission agreed to relax rules on processing slaughtered beef on the bone.
Beef may now be taken off the vertebral column of animals up to 30 months old, rather than 24 months previously due to the decreasing risk of BSE or Mad Cow Disease.
Liz Lynne, MEP for Shropshire and West Midlands and Lib Dem European agriculture spokesperson for England and Wales, welcomed the decision which she said would benefit the meat industry.
She said: “This decision is good news for local farmers and consumers alike as it shows increasing confidence in the safety of our meat and its producers. Extensive research shows that the fight against BSE is being won and it is right the rules should be adjusted accordingly.
“The changes will improve the competitiveness of our meat industry and reduce waste disposal costs as less needs to be classified as ’specified risk material’ and destroyed.
“The new rules also bring us into line with the international standards set by the World Organisation for Animal Health.”
The strict controls were brought in to improve food safety but also had the effect of increasing costs for farmers and processors, as well as reducing the supply of bone-in cuts to customers.
One Comment
You wrote; “Beef may now be taken off the vertebral column of animals up to 30 months old, rather than 24 months previously due to the decreasing risk of BSE…”. Yes, very good. However, where is „mad cow risk“? What’s scarier than mad cow disease? Nothing, really — except illnesses that are 10 billion times more likely to hurt you. Think about it this way: Your risk of getting mad cow is much lower than your odds of winning the Powerball lottery… says Marc Siegel, M.D., a clinical associate professor of medicine at New York University Medical School (http://www.cnn.com/2007/HEALTH/06/14/healthmag.diseases/index.html?eref=rss_health).
I described an alternative “BSE ammonia-magnesium” theory (http://www.agriworld.nl/feedmix/headlines.asp?issue=3). This theory is based on the chronic Mg-deficiency- potentiated by hyperammonemia (high protein intake?). These mechanisms have a strong influence on CNS, especially in ruminants and carnivora animals (www.bse-expert.cz).
There will be no epidemic of the human form of mad cow disease in Britain, despite fears that the worst is yet to come, recently (September 2007) an expert said. We are “highly unlikely” to see a resurgence in the fatal brain condition, according to Professor Bob Will, director of the National CJD Surveillance Unit, who was speaking at a medical conference in Edinburgh (PRION 2007) (http://theherald.co.uk/mostpopular.var.1717677.mostviewed.epidemic_of_vcj d_in_uk_highly_unlikely.php).
Professor Brown, lecturer and researcher at the University of Bath, is another dissident scientist who believes the entire BSE/CJD link must be completely reconsidered. His research team recently found that elevated manganese (Mn) was associated with prion infection. These findings, published in the Journal of Animal Science, also show the possibility of using Mn levels in the blood as a potential diagnostic marker for prion infection (http://jas.fass.org/cgi/content/abstract/85/6/1596).
However, these findings about “BSE; manganese theory”act in concert with my “BSE; ammonia- magnesium theory”. So, I will perform some interpretations in my website with conclusion; why some central nervous system regions showed elevated Mn, other regions did not? and why the most consistent finding was an elevation of Mn in blood? However, in the first place, this will be published- presented at the 29th World Veterinary Congres (Vancouver, July 27-31, 2008), see article; Neurodegenerative Diseases and Schizophrenia as a Hyper or Hypofunction of the NMDA Receptors (http://www.meet-ics.com/wvac2008/pdf/PS1-17Mar2008.pdf).