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Age of Positives Rising in UK

Kathy

Well-known member
Mike
these stats cannot be considered complete, since during the foot and mouth outbreak in 2001 over 400,000 cows were destroyed and burned (on Canadian rail-road ties full of creosote). These animals were not tested for BSE. We will never know how many more, born after the re-inforced feed bans (BARBs) occurred within this large group of cattle.
 

Kathy

Well-known member
From the link you gave, Mike, I went to a few other DEFRA sites. The link below was quite interesting. This is a selected quote taken from the page which was last updated Oct 25/05.

It is totally ignoring the work done by Brown, et al. which demonstrates that the healthy prion protein's job IS to balance copper (copper homeostasis) in the brain, and provide copper for anti-oxidant enzymes, of which the prion protein has also been demonstrated to be.

It is also totally ignoring the environmental metals factor which was identified by Mark Purdey, researched by others like Brown, Ragnosdottir, Chalet, Wong, etc. etc.....

There is no mention of the environmental factors which influence the development of TSEs under this "Causal" reference. While some of the work which is out now, may not have been published at the end of October 2005; the government was certainly aware of it. (FATEPRIDE)

What do you do when the government propaganda is so biased? What can we do, when they ignore the research which is, by far, more plausible than the "infectious protein" hypothesis.

When the UK government makes such statements as "not.. all novel hypothesis will be tested..." everyone should be screaming "foul". If they were as unbiased as they try to say they are, then they would pay for the testing of other novel hypothesis. Instead, they hide behind the lies which they have perpitrated in order to prevent liability against their forced use of the copper chelator "Phosmet" in their government mandated warble eradication program. Not to mention, the contamination of the environment with metals, and radio-active contaminants from various industries.


http://www.defra.gov.uk/animalh/bse/science-research/pathog.html

Causative agents of TSEs

There is still considerable scientific uncertainty about the precise nature of the causative agents of TSEs. The prion protein PrP is a normal membrane-associated protein that is found most commonly in the central nervous system and is very important in the development of TSEs. Modified forms of this protein are associated with infectivity and also accumulate in the brain in the diseased state. The function of the unmodified prion has not yet definitively established.

Put simply, the prion hypothesis says that infectivity is caused by a structurally-modified form of the PrP that promotes conversion of other PrP molecules into the same form. These then accumulate to interfere with the function of nerve cells. However, whether the prion (the PrP protein alone, with no associated nucleic acid) is the cause of BSE is not certain.

Other theories suggest that the causative agent might be a "virino"; an infectious pathogen containing a core of nucleic acid associated with host derived cellular proteins, similar to a small virus. Alternatively, some scientists have argued that a filamentous virus is the cause of TSE.

The prion hypothesis may be the most popular at present, but a number of scientists find difficulties with it, primarily as it contradicts the scientific orthodoxy that the inheritance of a trait, such as disease, must be associated with nucleic acid. MAFF holds no particular position with respect to the nature of the agent as all hypotheses currently remain unproven. This does not, however, mean that all novel hypotheses will be tested by research as most can be tested for a fit with current scientific knowledge about BSE.

This scientific uncertainty over the nature of the causative agent does not, however, affect the validity of the steps taken to control the disease and protect human health. The basic tenets on which the controls were based, namely, that the infective agent is transmitted through contaminated feed and detected only in certain tissues, even in clinically affected animals, apply, whatever the actual form of the agent.

(Page last modified: 25 October, 2005)
 

Kathy

Well-known member
http://www.defra.gov.uk/animalh/bse/index.html this separate page, the homepage for BSE, was last modified: 5 July, 2006

Under the latest developments, there is STILL NO REFERENCE to the involvement of metal bio-availability and prion disease.

This is a flagrant denial of the truth!

Bioavailable copper and manganese in soils from Iceland and their relationship with scrapie occurrence in sheep.
K. Vala Ragnarsdottir *, Darren P. Hawkins
Abstract
The bioavailability of trace metals can be directly linked with many common animal and human diseases. It is easier to correlate
regional geochemical trends with disease distribution in the developing world because local populations and animals live from the
land. In the western world, humans tend to live from the global food market whereas animals graze on the land. Recent biochemical
studies have shown that the prion protein needs copper to keep its structure. If copper is not available, the prion protein can take up
manganese and unfold. Preliminary results for trace metals in soil samples from scrapie-affected areas in Iceland show that
bioavailable manganese manganese (easily reducible and exchangeable Mn) is very high whereas soluble copper and free copper
are very low.

EXPOSURE TO SOIL HIGH Mn AND LOW Cu CONCENTRATIONS AND THE DEVELOPMENT OF SCRAPIE
G. Roman-Ross, L. Charlet #, F. Eychenne, G. Perfetti and G. Ru
Abstract
There is clear evidence that the occurrence of prion diseases often has a non-random distribution, suggesting a link to some environmental factors. Purdey (2000) and Brown et al. (2000) have suggested that sporadic prion disease could be linked to environmental or dietary deficits of Cu in the presence of high Mn. Analysis of regional variation in local manganese/copper levels were determined and compared to the incidence of the diseases. Our results show for all the soils samples from scrapie-affected farms, high concentrations of bioavailable manganese (exchangeable and easily reduced) and very low concentrations of soluble and free copper. These observations are therefore supportive of the hypothesis that excessive dietary Mn linked to a hypocupraemia could contribute to scrapie development.

Thankfully, MAFF and DEFRA have not stopped all research under "environmental factors".
 
A

Anonymous

Guest
I guess the main thing that stuck out to me is the number of UTM's (under thirty months) that had tested positive...

And yet still the USDA is using 30 month as the magical number month where they can't occur any younger- and accepting BSE beef and cattle 30 months old from a country with a much higher rate of BSE- while our customers who know better won't accept anything over TWENTY months old :???:
 

Mike

Well-known member
Thankfully, MAFF and DEFRA have not stopped all research under "environmental factors".
Ditto! Even the Russian Dr. at Auburn Univ. (can't remember his name) is working feverishly along these lines, or so I'm told.
 

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