BSE disposal of specied risk material nightmare

[Kathy]

Last December 2007, I sent a copy of Mark Purdey's new book "Animal Pharm" along with a couple of DVD documentaries Mark and on "depleted uranium" to my AB Agriculture Minister (G. Groenveld).

I also included a letter which expressed my deep concerns about how Specified Risk Material is being mixed with contaminated soil from the Oil and Gas industry, and buried in a landfill at Coronation, AB. The plans are to build an incinerator (or so a news article stated) that will later burn this stored SRM/waste in a high temperature incinerator (like Swann Hills). Nobody asked the neighborhood if we wanted it!

I recently spoke with an owner of a small butcher shop, who informed me that only the SRMs from Cargill and Tyson are going to Coronation. That all the rest of the SRMs from AB and SK are being sent to Saskatoon to be incinerated. After incineration, the "ash" is then trucked to Rimbey and buried in a landfill there, where (he said) it is guarded 24/7.

Why the need to protect, or prevent, access to the "SRM ash"? Certainly, after burning this material at high temperatures, there would be NO PROTEIN material left. Only the metals and minerals would remain.

After sending a letter to Groenveld, the CFIA and AB Veterinary Department in June 07, the book 'Animal Pharm"/DVDs to GG in December 07, and a follow up email to GG in April 08 (as I had not heard from GG to know if he had received the package in Dec)...... I got my own package in the mail from the Hon. GG - RETURNING Mark Purdey's book and the DVDs.

Here is what the Hon. Minister of Agriculture stated:

"May 12, 2008

Dear Mrs. Czar:

Thank you for your April 20, 2008 email regarding a package you sent to my constituency office in December 2007. I apologize for the delay in responding to you. The package has now been located and I have reviewed and shared the enclosed material with the Office of the Chief Provincial Veterinarian.

The true origin of transmissible spongiform encephalopathies is unknown at this time. Many different theories about the cause and pathogenesis of these diseases have been advanced, and it is possible that many factors interact to result in disease development.

Current scientific evidence strongly supports the theory that the infectious agent for bovine spongiform encephalopathy (BSE) is composed largely of a prion transmitted through the consumption of BSE-contaminated food products. This consensus is the basis for removing and destroying specified risk material (the prion containing tissues) at the source, thus alleveating any possibility of cross-contamination of animal feed products. However, Agriculture and Rural Development will continue to monitor the scientific literature related to BSE and other issues impacting agriculture, and adjust our policies and regulations accordingly as theories are validated by further study and research.

Please find enclosed your copy of Mark Purdey's "Animal Pharm" and the two DVD documentaries. I appreciate the opportunity to review this material and I commend your initiative in investigating issues which may impact your livestock operation. Agriculture and Rural Development will continue to support BSE research and other animal health initiatives as key elements of growing sustainable agriculture in Alberta.

Sincerely,
George Groenveld
Minister
enclosures"


So there you have it!

The true origin of transmissible spongiform encephalopathies is unknown at this time.

And it will never be "known" because the people/docs heading up the Alberta Prion Institute (Dr. David Westaway) refuse to admit the importance of copper to the well-being and proper formation of the healthy prion protein. Dr. Westaway was very rude at a recent CWD meeting, where-in I attempted to bring forward the work of Dr. Vitaly Vodyanoy of Auburn University in Alabama (see USA patent application 20070122799) for an example.

Dr. Westaway declared copper "unrelated to prion disorders" and then insulted the integrity of any research/researcher coming from Alabama.

CWD in wild deer and elk "in Alberta" have been diagnosed based on positive tests of the lymph glands in the neck - for the "most part", according to Dr. Margo Pybus. There is a problem here, as CWD positive animals should also show "pos" in the brain tissue - but many cervids (in AB) have not. So tell me, do they actually have CWD, or are they battling against an "environmental toxin" such as "depleted uranium" or "tungsten" particulate that is causing their immune system and lymph system to work overtime to eliminate subsequent "malformed proteins".

As the Hon. Minister states, "...it is possible that many factors interact to result in disease development."

But, because the reknown BSE/prion researchers of the UK have told us that the "infectious agent" was in the feed we are dealing with a very costly SRM removal and disposal system. Even though their "transmission experiments" absolutely fail to imitate real-life situations; and "contaminated MBM" feeding trials in the UK failed to induce BSE in any animals. (read Animal Pharm) I've donated a couple dozen to Alberta libraries.

Small butcher shops across this country are being forced out of business because of the costs they must pay to "ensure the safety of our food". Is not this cost in the interest of the public good? Are not the procedures they must follow, IMPOSED by a government/CFIA that ADMITS - "The true origin of TSEs is unknown at this time."

So tell me, why are the small butcher shops paying for this "safety measure", for that matter why force Cargill and Tyson too? Wouldn't it be cheaper to test the animals? (Using the BIO-RAD test kit developed by the French Atomic Energy Commission: BIO-RAD stands for "Radiation-Biology" in french - so its flipped around).

Disposal of SRMs in the manner which is presently taking place is a FARCE. As one butcher stated, "Its basically saying you can eat the inside of a piece of bread but all the crust is poison."

For all my efforts (and Mark Purdey's) to investigate the TRUE multifactor cause of BSE, I am given a pat on the head and a door slammed in my face. The two DVDs I sent to GG were:

"Mad Cows and an Englishman" (a doc. about the early findings of Mark Purdey), and

"The Doctor, The DU and the Dying Children" a doc. about how depleted uranium from conventional weapons (bullets, bombs and bunker busters) used in Iraq and Afganistan have polluted the environment and are causing the death and disease of those unfortunate enough to be exposed to the depleted uranium (inhaled nanoparticles, consumed in food and water, or adsorbed via the skin).

I note, Minister GG did NOT mention "depleted uranium" in his response. Neither has he offered to investigate the use of depleted uranium weapons at CFB Suffield, Wainwright, or Cold Lake.

Also, why did it take my follow-up e-mail of April 20, 2008 for GG to "locate" my package sent in December 2007?

I have to wonder who actually reviewed this information (the book and the DVD documentaries).

This information is posted here so that you can make some of your own conclusions. When valid scientific data is brought forward to our government, CFIA and the Office of the Chief Provincial Veterinarian (of AB)... their response is thus.

They continue to "inject brain homogenate" into the cranium of animals to determine the cause of BSE and other TSEs. This is NOT based on the feeding of MBM. Direct injection into the brain, reflects "inhalation" (especially directly through the olfactory system/nose) not "consumption".

If anyone cares for more information on this subject, I will gladly supply it to you (ie: how the inhalation of rogue metal nanoparticles is contaminating the prion protein and causing its malformation, thus its inability to function properly causes a cascade of oxidative damage that destroys the viability of the cell)... You can also search the "Entrez Pubmed" medical search engine for Oxidative Stress, metals, Mark Purdey, David R. Brown, F. Paquet and prions.

Our government has left us to the whims of a CFIA that bases its BSE prevention criteria on the findings of researchers that have corrupted the science - to protect whom?

[wilagro]

I will believe the CFIA findings UNTIL there is a more plausible scenario.

Contaminated bone meal from Great Britain sold all over the world (including North America), was a common vector for spreading the causative agent of BSE. The processing of bovine waste into material added to feed concentrate to provide cheap protein, compounded the problem by mixing and distributing contaminated feed. This practice should never have been allowed at any time.

Depleted Uranium...stretching the bounds of plausibility in my opinion.

Heavy metals...I would like to see more research as to their place in this puzzle, if any.

My opinion on the BSE phenomena, others may disagree.

[per]

You won't find anyone who thinks it is OK to feed animal protein to animals but how do you explain CWD in wild deer. Not too many of them were fed by anyone anything other than what is natural and existing in the environment. Notwithstanding, Kathy's point of testing would be cheaper than hauling the SRM's back and forth is quite valid.

[wilagro]

per: From what I read CWD is similar but not quite the same as BSE.

One possibility in the spread of CWD are common natural salt licks where saliva (fresh or dried) from one animal could be picked up by another animal. That is probably a long shot although someone suggested that the same thing could happen with grass. Nobody really knows. So far there have not been many whitetail deer infected here (east-central AB), although a few were found last fall in Alberta along the border with Sask. More deer infected in Sask. so far...but that could change also.

Testing for BSE would be a good thing if the tests could be proven to be accurate for young as well as older animals and less costly than disposal of SRMs.

[tman]

The one specific question that I have never seen come up is "how did BSE originate?" Now lets assume that the whole contaminated feed thing is true and accurate. How did these prions form initially? At some point the very first infected animal that was ground up and fed back to its pen mates had to have been "infected" by some other form. All that CFIA etc has theories on is the spread, NOT the cause.

[wilagro]

I presume that conditions were right for the first "mutation" or abnormal formation of prions. Somewhat like the flu virus does.

Anyway the abnormal prions seem able to replicate themselves when introduced to another animal (or human).

This is science way above my understanding and we can only hope that researchers will solve this puzzle.

[rkaiser]

Thanks again Kathy for all of your effort.

Can't really expect much more out of poor old GG. He is taking lead form many people in his position as he cannot possibly learn everything about everything. Sometimes the lead person has his / her own agenda and that is painfully obvious in this case.

[farmers_son]

From Animalnet:

ONTARIO: U of O research examines risks of mad cow disease
21.may.08
Ottawa Business Journal
Julie Fortier
http://www.ottawabusinessjournal.com/2976772642041.php
It may be hard to believe that although bovine spongiform encephalopathy (BSE), or 'mad cow disease,' has cost the Canadian economy around $10 billion in lost trade and compensation, little is known about the disease.
This month, PrioNet Canada, a federally funded network that studies prion-based diseases like BSE, moved to change that by announcing $590,000 in funding for two related projects at the University of Ottawa.
The funding is part of an $8-million injection into 19 projects across the country examining prion diseases and their effects, and will fuel research conducted by U of O's Dr. Daniel Krewski and Dr. Michael Tyshenko.

See PrioNet at:
http://www.prionetcanada.ca/

The Canadian Cattlemen's Association is one of Prionet's partners as well as universities across Canada, The Alberta Prion Institute and the Canadian Food Inspection Agency.

[grassfarmer]

Thanks Kathy for keeping up the battle! I'm interested (and horrified)that the BSE ash is being hauled to Rimbey - i'll try and dig up where it's really going.
Tman - the original "theory" in the UK was that BSE originated by a cross species contamination of feeding remains of scrapie infected sheep to cattle. They seem to have dropped that story of late.
As you say the feed theory needs to have had an original cause and this has never been proven. Where I would disagree with Kathy, and Mark, was that there was no transmission of BSE through feed in the UK. I think that Mark did some sterling work on the causes of BSE and probably got closer to the truth than anyone else has but having lived through BSE in the UK and seeing the spread/speed factor of it I am firmly convinced that it was spread for a period through the calf milk replacer. How else do you explain that it was virtually confined to dairy farm reared stock - several beef breeds never had a case. The first case in the Galloway breed was on a farm close to me - a farm that also had a dairy herd and the cow in question had been orphaned as a calf and reared on milk powder with the dairy replacements.

[Kathy]

The milk replacer has high levels of manganese.

The feed, MBM, (especially in UK and other EU countries) at the time of the huge BSE situation, was contaminated with chemicals from the Organophosphate treatment of cattle.

As for the prion causing the disease, and replicating on its own? Don't believe everything you hear. Next time old Bessy injects homogenized brain tissue into her little brain, then the CFIA's transmission theory might be considered plausible.

The Blood Brain Barrier protects the brain. However, inhalation of extremely small particulate can bypass the BBB and go directly to the brain via the olfactory system.

The cattle/deer et al. that are feeding will inhale alot of particulate fromt the feed or soil due to their anatomy.

I wish I could show everyone hear all the research I have dug up on the subject. I can only express to you that I have seen enough to be convinced this is a metal/mineral contamination problem - and absolutely not an infectious disease.

The feeding trials that are claimed to show transmission of prions do not. They show that something that was in brain material of diseased animals, when specially treated and highly concentrated, then drenched into the stomachs of a few bovine calves - caused some but NOT all the calves to have a positive test, which identifies specific amino acid sequences that are NOT specific to only malformed prion proteins. In the Terry, Wells study, the researchers had to pool tissue samples in order to get this positive.

If feed were the agent of tranmission, there would be millions of cases throughout the world, as Mark pointed out, especially in the Arab Emerits - as they imported the most of this feed.

By tricking people that they are getting this disease from a mysterious prion protein in feed, the real cause is being ignored - but thankfully NOT by everyone.

Meanwhile at the AB Prion Institute, we have Dr. Westaway telling people that copper and the prion protein have no relationship with each other. This is a flat out lie!

These researhers (abstract below) have shown that a "ferritin" (iron) based molecule/metal nanoparticle-based, was capable of distinguishing/separating man-made prion peptides via the region which is supposed to bind copper.

Copper is not magnetic, and in order for the columns to capture the peptides, other metals must be bound to this region - which are paramagnetic.

Uranium and other heavy metals, when lodged in the body (usually attached to proteins) cause much damage from what's called the "chemical effect" (not radiation).

Dr. Chris Busby of the UK, has shown how this effect is happening. He has demonstrated the "photo-electron effect" where the various metals/minerals absorb and amplify back-ground radiation (being everything from sound, light, UV - gamma et al.).

In a study in 2007 by Elsaesser et al. the researchers used a "CERN Monte Carlo model" to pattern the effect of predicted enhancement of gamma and x-rays with various metals vs. H20

They demonstrated that the absorption of gamma and x-ray was proportional to the 4th power of the atomic number. With a water molecule (H20) having an atomic weight of 3.33 it had an enhancement effect of 1 (one).
Calcium effect = 1220
Strontium effect = 17,073
Barium effect = 79,675
Gold effect = 308,943
Uranium effect = 585,365

In this model, when water was exposed to 100,000 photons there were 4 tracks of electrons shooting off of it.

With Gold and Uranium, under exposure to ONLY 1,000 photons there were SIGNIFICANTLY more electron tracks shooting out of the metal nucleus.

This demonstrates how these heavy metals are capable of releasing electron energy in a form which is directly related to energy input. This is a CASCADE EFFECT!

Also, for decades it has been known that uranyl ions (the most common form of uranium in human blood) have an affinity for DNA. Depleted uranium (uranyl acetate, for example) is used as a laboratory stain for DNA. Under very, very low concentrations, uranium will saturate DNA. This has an effect on the ability of the cell to produce healthy proteins, including repair proteins.

An example of exposure to LEAD in dogs, (abstract below) demonstrates how this heavy metal was capable of causing spongiform in the brain. Dr. Amir Hamir did this study in 1984. He is presently working on CWD, in the US. The low calcium died, allowed the lead to take the place of calcium in the dogs body.

I'm not saying only depleted uranium can cause these diseases; tungsten and lead, barium, strontium - all these other rogue metals which enter the body and "stick" are causing problems, (not just TSEs). However, the thing with "burned" or "incinerated" metals, is that they vapourize with specific temperatures/metal and recondense into "insoluble" metal nanoparticles.

DU weapons and bombs create unfathonable amounts of these insoluble metal/metal alloy particles. When they stick in the body, they cannot be eliminated the same as natural/non-fired metals. Our bodies don't know how to handle them very well. They stay lodged where-ever they are and they very very slowly, release metal ions from the particle. They ALSO absorb and enhance background radiation in an "atomic weight" and "particle size" relationship. The smaller the insoluble particle, the more trouble as it can float through the body unimpeded, and lodge anywhere. Having an affinity for DNA, uranium is EXTREMELY dangerous - thus it should be left in the ground, undisturbed.


J Comp Pathol. 1984 Apr;94(2):215-31. Links
Neuropathological lesions in experimental lead toxicosis of dogs.Hamir AN, Sullivan ND, Handson PD.
Light microscopical examinations were carried out on the central and peripheral nervous systems of 9 dogs maintained on a high-fat-low-calcium diet and dosed orally with a mixture of lead chloride, lead bromide and lead sulphate. Microscopic lesions were present in 7 (78 per cent) of the lead-treated dogs. Cerebrocortical lesions comprising spongiosis, vascular hypertrophy and gliosis predominated. These lesions were bilateral, had a predilection for gyri and were located mainly in the parietal and frontal cortex. There were bilaterally symmetrical spongiform changes in the brain stem. The cerebellum had spongiform changes in the roof nuclei and in the lingula there was spongiosis of the Purkinje cell layer and vacuolation of Purkinje cells. Axonal degeneration was evident in a sciatic nerve of one dog. In a second experiment, designed to study the early ultrastructural changes in the brains of dogs with lead intoxication, 2 groups of dogs, one on a commercial balanced diet and the other fed a high-fat-low-calcium diet, were given similar amounts of lead. Cytoplasmic accumulation of lipid was found in the cerebrovascular pericytes of all dogs treated with lead but vascular changes were otherwise not obvious. Quantitative evaluation of numbers of blood vessels by light microscopy revealed an apparent increase in all dogs receiving lead. This increase in vascularity was greatest in the dogs fed the high-fat-low-calcium diet.

PMID: 6736309



Chem Res Toxicol. 2007 May;20(5):784-9. Epub 2007 Apr 14. Links
Uranyl acetate as a direct inhibitor of DNA-binding proteins.Hartsock WJ, Cohen JD, Segal DJ.
Department of Pharmacology and Toxicology, University of Arizona, Tucson, Arizona 85721, USA.

Zinc finger proteins, one of the largest families of DNA-binding proteins in higher eukaryotes, are so named because they require zinc ions for appropriate structure and function. Dysregulation of zinc finger-containing DNA transcription and repair proteins has been proposed as a potential mechanism for the toxic effects of some metal ions. Uranium metal has been reported to be both a cytotoxic and a genotoxic agent. We hypothesized that these toxic effects of uranium might be due to its ability to directly disrupt zinc finger activity. To test this hypothesis, two purified zinc finger proteins, Aart and Sp1, were analyzed by electrophoretic mobility shift in the presence of uranyl acetate. Inhibition of binding was apparent at 10 microM uranyl acetate, while no inhibition was observed with up to 2000 microM the cytotoxic metalloid sodium arsenite. Preincubation of the DNA with uranyl acetate did not inhibit zinc finger protein binding, suggesting that the inhibition was due to direct uranyl interaction with the protein. Surprisingly, uranyl acetate inhibited two nonzinc finger DNA-binding proteins, AP1 and NF-kappaB, to a similar extent, and zinc finger inhibition was reduced in the presence of bovine serum albumin. These results suggest that uranium can directly inhibit the function of DNA-binding proteins, most likely via a nonspecific protein interaction.

PMID: 17432879



Anal Biochem. 2007 Jul 1;366(1):1-8. Epub 2007 Mar 13. Links
Nanoengineered analytical immobilized metal affinity chromatography stationary phase by atom transfer radical polymerization: separation of synthetic prion peptides.McCarthy P, Chattopadhyay M, Millhauser GL, Tsarevsky NV, Bombalski L, Matyjaszewski K, Shimmin D, Avdalovic N, Pohl C.
Research and Development, Dionex Corporation, Sunnyvale, CA 94088, USA.

Atom transfer radical polymerization (ATRP) was employed to create isolated, metal-containing nanoparticles on the surface of nonporous polymeric beads with the goal of developing a new immobilized metal affinity chromatography (IMAC) stationary phase for separating prion peptides and proteins. Transmission electron microscopy was used to visualize nanoparticles on the substrate surface. Individual "ferritin" molecules were also visualized as ferritin-nanoparticle complexes. The column's resolving power was tested by synthesizing peptide analogs to the copper binding region of prion protein and injecting mixtures of these analogs onto the column. As expected, the column was capable of separating prion-related peptides differing in number of octapeptide repeat units (PHGGGWGQ), (PHGGGWGQ)(2), and (PHGGGWGQ)(4). Unexpectedly, the column could also resolve peptides containing the same number of repeats but differing only in the presence of a hydrophilic tail, Q-->A substitution, or amide nitrogen methylation.

PMID: 17481564