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Ranchers.net

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.
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