• If you are having problems logging in please use the Contact Us in the lower right hand corner of the forum page for assistance.

Interview with Danny Matthews on BSE

Kathy

Well-known member
Innovation Alberta has some transcribed interviews with various doctors regarding TSEs.

Lots of infectious comments!

Link to entire article:
http://www.innovationalberta.com/article.php?articleid=683

A comment by Dr. Matthews caught my eye:

CC: YOU WERE ASKED TO ADDRESS SOME OF THE GAPS IN TERMS OF OUR KNOWLEDGE ABOUT THESE PRION-RELATED DISEASES. WHAT IS IT THAT WE STILL NEED TO ADDRESS, WHAT ARE THE IMPORTANT QUESTIONS?

DM: Well, the big unknown is still what is the agent. We tend to refer to prion almost as if in common language it actually means something but the bottom line is it still relates to what is thought to be an infectious protein. But where there is still some occasional conflicting data and to me that is the key finding for all of these prion diseases–humans and animals–can we actually identify what causes that disease, how it can be transmitted from animal to animal would be better understood if we could do that and there is evidence, for example, that they are not universally transmissible from animal to animal or human to human. And understanding the make-up of the agent would actually help you understand that. Why it happens. Why it doesn’t happen. And, how you could then control it.

I think this is a very telling paragraph. It is in amongst alot of speculation and theory about "infectious prions". But this paragraph does tell the truth; they don't know what the causal agent is.

Dr. Matthew's also commented right off the start:

the first things we had to try and prove was that the disease we were dealing with was a transmissible disease, that it could be transmitted particularly to mice and to cattle experimentally and that it wasn’t just the result of a toxin or a poison that had gotten into feed and that it was generating a neurological disease. Once we knew that it was infectious then we clearly were dealing with something that was going to have a much longer life span than a toxic event would have where you might have one batch of feed that was contaminated and then subsequently it would be eliminated.

Sadly, the assumption that a toxic element could only have occurred in only one (or say a handful) of feed batches was their first mistake. The toxic agent (metals) were prevelent in all the meat and bone meal at levels low enough to not cause an immediate acute reaction. Their build up was accummulative over a long period of time.

So was the contamination by organophosphates. Low levels in the rendered fats breezed by the new rendering procedures into the feed. Results, animals exposed to chronic low level OPs. This would have a insidious copper chelating effect that robbed the animals of their bio-available copper.
 

Kathy

Well-known member
Here is a letter to the editor from Mark Purdey. It is a couple years old, but the situation remains the same:

Letter from Mark Purdey to the 'Farmtalking' forum 12 July 2004
Hi folks,
Last Sunday, the New York Times reported the US government's intention to totally ban the feeding of farm animals back to farm animals to eradicate any future risks of mad cow disease.

But by banning the feeding of farm livestock to farm livestock, The US officials really have missed the true cause of mad cow disease. Its not that I personally support the feeding of meat and bone meal to farm livestock - an abhorrent practice that one could hardly wish to see continued - but it does not represent the true cause of this disease.

When we banned the feeding of Meat and bone meal in the UK in 1988, 40,000 cattle have still gone on to develop BSE despite being born after this ban. Furthermore, during the 1960s, 1970s, 1980s, 1990s, Britain exported thousands of tons of this supposedly 'infected' meat and bone meal to continents like Africa, India, south America, the Middle and Far East, yet not a single case of mad cow disease has erupted to date. A schoolchild could see the stupidity of connecting the feeding of this feed and the origin of BSE

addendum in later posting (...why no BSE in so many countries that purchased boatloads of our meat and bone during the BSE ( post 1986 ) era? This is what I cannot work out. Well, thinking about it now, perhaps it was because no other country except for the UK had the exclusive high dose systemic organo phosphate which opened up the blood brain barrier and allowed the Sr 90 crystals through into the CNS . That could be the all important triggering factor. that determined why the UK got it the worst, followed by the other countries like Switzerland, Ireland, France , Portugal, which were eradicating warbles using half the dose rate.
In fact, many farmers , plus myself included, had noticed this curious bone wastage syndrome that seemed to run in tandem with the progression of BSE. Also excessive bouts of milk fever in cows ( hypocalcaemia ) that could not be cured by the standard bottle of calcium would erupt in cows several months before the symptoms of BSE emerged. Again, this implies a strontium 90 replacement of calcium / magnesium in the bone matrix and the calcium channels involved in the hypocalcaemic milk fever syndrome. It would also explain why the calcium infusion would not work as a treatment, as the sites had become occupied by the alien invasion of strontium 90.

Interesting stuff.)

The scrapie agent in the feed merely represented an ideal misappropriated scapegoat for which no big corporation or government interest could be held accountable for damage claims. Many officials here in Britain will admit to this in a private capacity. Even Ministers have personally informed me that no one knows what the true cause of mad cow is.

My own global analytical research has recently amassed sufficient analytical data that conclusively indicates that exposure to certain environmental metal microcrystal pollutants are responsible for the true cause of these diseases. These involve either barium, strontium 90, silver or manganese and are released into the environment from various naturally occurring ( volcanoes, etc ) and man made ( military, industrial, etc ) sources. Exposure to each different metal species dictates which specific 'strain' of the disease will emerge.

Once implanted in the brain, these crystals seed the multireplication / growth of significant sized metal-protein crystal arrays ( the heat resistant fibrils which hallmark the BSE diseased brain) , which behave much like the piezoelectic crystals found in microphones , thereby screwing up the ability of the organism to deal with incoming sonic pressure waves. The sound energy is converted into electrical shock bursts which, in turn, initiate free radical mediated neurodegeneration and mad cow disease.

It was the release of strontium 90 into the atmosphere from the April 1986 Chernobyl nuclear plant blow out that rained down over North western Europe and contaminated their pastures. This radioactive metal microcrystal was able to penetrate the brains of cattle because of the simultaneous use of a high dose systemic acting pesticide used uniquely for warble fly eradication here in the UK. The chemical disrupted the protective blood brain barrier of the treated cattle, thereby allowing the strontium 90 microcrystals to leak into the brain, and kick off the deadly mad cow melt down.

The one US mad cow was just down the road from Hanford nuclear weapons processing plant. Likewise the main US cluster of CWD ( spongiform disease ) in deer that kicked off in 1967 is focused in the area downwind of the prolonged radioactive leak that issued from the Rocky Flats nuclear weapons factory ( during the second half of the 1960s). Furthermore, the deer which first developed CWD had originated from the very same pens at the US government's Fort Collins facility which had been experimentally exposed to these radioactive emissions for the purposes of scientific monitoring the impact of radioactive metals on the mammalian biosystem.

Other TSE clusters I have researched in the US involved the development of CJD in the human workforce of a nuclear / conventional missile factory in Tucson Arizona, whilst further TSE clusters have developed where these missiles were test fired at White Sands Missile Range ( New Mexico ) and up at Cold Lake air weapons range on the Albertan/ sakatchewan borders in canada - exactly where the first Canadian case of BSE originated from. And the correlations go on and on.

My latest analytical results have confirmed the disturbing fact that this toxic phenomena clearly represents the true cause of these diseases. But governments remain totally negligent in respect of serving the public interest. They will never publically admit to it , for obvious reasons.

Best,

Mark Purdey
 

Latest posts

Top