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BSE caused by oxidative stress and metal imbalance

Kathy

Well-known member
Neurotoxicology. 2006 Feb 13;

Free radical generation of protease-resistant prion after substitution of manganese for copper in bovine brain homogenate.

Deloncle R, Guillard O, Bind JL, Delaval J, Fleury N, Mauco G, Lesage G.

Universite Francois Rabelais de Tours, Bio-Inorganic Chemistry Laboratory, Faculty of Pharmacy, 31 Avenue Monge, 37200 Tours, France.

The exchange between copper and seven transition metals is studied in a bovine brain obex homogenate according to the redox status of the medium. In reductive conditions, almost all the studied metals can substitute for copper when it is in the reduced form Cu(+). This substitution is reversible, since copper uptake as Cu(++) is restored in an oxidizing medium but only Co(++), Ni(++) and Mn(++), in this decreasing order, can substitute perfectly for copper in bovine brain homogenate. To study free radical effects on bovine brain proteins, at first a copper substitution was processed in order to inhibit superoxide dismutase-like protective properties against free radicals in copper metalloproteins. Manganese was selected since a brain copper decrease correlated with a manganese increase is well-known in transmissible spongiform encephalopathies. Results for bovine brain homogenate, initially negative in the Western blot Prionics((R)) test, indicate that the substitution of manganese for copper in a reducing medium and exposure to UVA-induced free radicals produce proteinase K resistant prion. These findings suggest that an impairment in brain metal homeostasis leading to oxidative abnormalities may be involved in transmissible spongiform encephalopathies.

PMID: 16481041

This isn't the newest study I was referring to that supports Mark Purdey's and others like Dr DR Brown - but it is another of many which are stacking up to support the causative relationship between BSE (prion disorders) and improperly balanced metals in the brain.

Free radicals and oxidative damage are responsible for nerve cell death. The self-defence mechanisms are exacerbated by the invasion of the brain by free-radical generating toxins.
 

Econ101

Well-known member
Kathy said:
Neurotoxicology. 2006 Feb 13;

Free radical generation of protease-resistant prion after substitution of manganese for copper in bovine brain homogenate.

Deloncle R, Guillard O, Bind JL, Delaval J, Fleury N, Mauco G, Lesage G.

Universite Francois Rabelais de Tours, Bio-Inorganic Chemistry Laboratory, Faculty of Pharmacy, 31 Avenue Monge, 37200 Tours, France.

The exchange between copper and seven transition metals is studied in a bovine brain obex homogenate according to the redox status of the medium. In reductive conditions, almost all the studied metals can substitute for copper when it is in the reduced form Cu(+). This substitution is reversible, since copper uptake as Cu(++) is restored in an oxidizing medium but only Co(++), Ni(++) and Mn(++), in this decreasing order, can substitute perfectly for copper in bovine brain homogenate. To study free radical effects on bovine brain proteins, at first a copper substitution was processed in order to inhibit superoxide dismutase-like protective properties against free radicals in copper metalloproteins. Manganese was selected since a brain copper decrease correlated with a manganese increase is well-known in transmissible spongiform encephalopathies. Results for bovine brain homogenate, initially negative in the Western blot Prionics((R)) test, indicate that the substitution of manganese for copper in a reducing medium and exposure to UVA-induced free radicals produce proteinase K resistant prion. These findings suggest that an impairment in brain metal homeostasis leading to oxidative abnormalities may be involved in transmissible spongiform encephalopathies.

PMID: 16481041

This isn't the newest study I was referring to that supports Mark Purdey's and others like Dr DR Brown - but it is another of many which are stacking up to support the causative relationship between BSE (prion disorders) and improperly balanced metals in the brain.

Free radicals and oxidative damage are responsible for nerve cell death. The self-defence mechanisms are exacerbated by the invasion of the brain by free-radical generating toxins.

Kathy, while you and flounder argue over the exact cause, it seems to me that in both cases the spreading of tses happens through the feeding of infected mamilian tissue. Is this correct?
 

flounder

Well-known member
kathy wrote;

BSE caused by oxidative stress and metal imbalance..........


:lol: :lol: :lol:


what a hoot, dream on there kathy, that is not what the study says.
you cannot even understand what you copy and paste. what it said was;

These findings suggest that an impairment in brain metal homeostasis leading to oxidative abnormalities

__may__

be

__involved__

in transmissible spongiform encephalopathies. ..........


NO WHERE did it state what you claim that;


BSE caused by oxidative stress and metal imbalance



kathy, you discredit yourself when you change the findings of the study and print things that are totally different from what the study claimed.


econ wrote;

Kathy, while you and flounder argue over the exact cause, it seems to me that in both cases the spreading of tses happens through the feeding of infected mamilian tissue. Is this correct?..............


that is correct econ, and as you probably already know, metals and ops are NOT infectious, but TSEs are.........tss
 

flounder

Well-known member
as i have stated time and time again, the origin is not important _to me_,
amplification and transmission is the key to stopping the spread. i have also always said that metals and or ops may/might play a role in susceptibility to the TSE AND they might not, but they are NOT transmissible as to be infectious. ...


Kathy wrote in another thread, but yet never documented;

> didn't say that OPs caused prion disease, but that they contributed greatly
> to the UK experience,

and again, could your please reference this materials with scientific data, instead
of hearsay please ???


you can argue the origin of TSE until all the mad cows on earth come home to roost.


i.e. ;


Phosmet induces up-regulation of surface levels of the cellular prion protein.
Neuroreport. 9(7):1391-1395, May 11, 1998.
Gordon, Irit 1; Abdulla, Elizabeth M. 1; Campbell, Iain C. 1; Whatley, Stephen A. 1,2
Abstract:
CHRONIC (2 day) exposure of human neuroblastoma cells to the organophosphate pesticide phosmet induced a marked concentration-dependent increase in the levels of PrP present on the cell surface as assessed by biotin labelling and immunoprecipitation. Levels of both phospholipase C (PIPLC)-releasable and non-releasable forms of PrP were increased on the plasma membrane. These increases appear to be due to post-transcriptional mechanisms, since PrP mRNA levels as assessed by Northern blotting were unaffected by phosmet treatment. These data raise the possibility that phosmet exposure could increase the susceptibility to the prion agent by altering the levels of accessible PrP.

(C) Lippincott-Raven Publishers.



http://www.neuroreport.com/pt/re/neuroreport/abstract.00001756-199805110-00026.htm;jsessionid=DOEcw0d3vPau1LEbPM42DrGrWVZnF06cF115hTGLe07ro2BZx8d3!586698740!-949856144!9001!-1





BUT, amplification and transmission is the most important factor in stopping the

spread of the TSE agent. WE have known for decades what factors involve the amplification

and transmission, yet the industries involved CHOSE to ignore this science until the incubation

period in humans and animals started to catch up with society.



would it not have been more easy and very much less expensive for MAFF/USDA et al to jump on the OP
bandwagon and save the industry, if OP theory had any credence to it at all? and why did they not?


transmission studies DO NOT LIE !

show me the data that ops are in all the primate/mouse transmission studies?


EUROPEAN COMMISSION
HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL
Scientific Steering Committee
OPINION ON
ORGANOPHOSPHATE (OP) POISONING AND
HYPOTHETICAL INVOLVEMENT IN THE ORIGIN OF BSE
Background
In its opinion on possible links between BSE and Organophosphates adopted on 25-26 June
1998 and in its opinion on Hypotheses on the origin and transmission of BSE adopted on 29-
30 November 2001 the SSC concluded that there is no scientific evidence in support of the
hypothesis of an OP origin of BSE.
The issue of organophosphate poisoning has not been dealt with by the SSC so far. The
concerns expressed in the enquiries cover mainly intoxication by occupational exposure of
shepherds and farmers to OPs upon use against ecto-parasites, especially in sheep dipping and
treatment of cattle against Warble Fly infestation. Risks from residues are addressed to a
lesser extend.
In early 2003, a large number of additional enquiries on the issue have been addressed to
European Commission’s Health and Consumer Directorate General. Four of these with
substantial enclosures were by one person. Most of them are addressing both issues: chronic
organophosphate (OP) poisoning and the origin of BSE.
Information provided with the enquiries
In addition to numerous newspaper and magazine articles the enclosures to the enquiries
provide the Material Safety Data Sheet on diazinon, the OHSA Occupational Safety and
Health Guideline for Tetraethylpyrophosphate (TEPP), an US agency Hazardous Substances
Fact Sheet on crufomate, company safety information sheets, some correspondence with UK
authorities including their activities to improve safe use of these chemicals. The information
regarding claimed OP chronic poisoning of cases presented does not provide evidence, neither
for OPs being the cause for diseases nor for their exclusion (i.e., “very low” bloodcholinesterase
levels, provided without data or comparison with the normal distribution of
values; successful treatment of a patient for OP clearance without giving any OP data). It
C:\WINNT\Temporary Internet Files\SSC_Last_OP_Final.doc 2
seems however, that due to insufficient, non-prudent use of the safety requirements undue
exposures of shepherds and farmers have occurred.
There is no additional information on the claimed involvement of OPs in the origin of BSE.
This applies for both, the hypotheses on the direct effect of OPs as well as on their
hypothetical role for Cu-deficiency to be involved in the origin of BSE (Cu binding of prion
protein is known). New publications are mentioned in one enquiry but they have not yet been
provided. In an Internet search no recent scientifically valid publications were traceable. The
SSC had been informed that research would be launched on this hypothesis, but no
information has been provided so far on its status or on results.
Conclusions
a) As regards the involvement of organophosphates in the origin of BSE, no new scientific
information providing evidence or supporting the hypothesis by valid data became
available after the adoption of the last opinion of the SSC on this issue. Consequently
there is no reason for modifying the existing opinions.
b) Regarding the possibility of OP poisoning, the European legislation for registration of
plant protection products and veterinary medicines – addressed in the enquiries – provide
the basis for safe use of registered compounds and their formulations. Regarding the
alleged intoxication cases reported and OP exposure it must be concluded that safety
measures may not have been strictly followed.
References
Brown, D.R., Qin, K., Herms, J.W., Madlung, A., Manson, J., Strome, R., Fraser, P.E., Kruck, T., von
Bohlen, A., Schulz- Schaeffer, W., Giese, A., Westaway, D. and Kretzschmar, H. (1997) The Cellular
Prion Protein Binds Copper In Vivo, Nature, 390, 684-7.
Purdey, M. (2000) Ecosystems Supporting Clusters of Sporadic TSEs Demonstrate Excesses of the Radical-
Generating Divalent Cation Manganese and Deficiencies of Antioxidant Co-Factors Cu, Se, Fe, Zn Medical
Hypotheses, 54, 278-306.
Scientific Steering Committee, 1998. Opinion on possible links between BSE and Organophosphates. Adopted
on 25-26 June 1998
Scientific Steering Committee, 2001. Opinion on Hypotheses on the origin and transmission of BSE. Adopted
on 29-30 November 2001.

http://europa.eu.int/comm/food/fs/sc/ssc/out356_en.pdf



Studies on the Putative Interactions between the Organophosphorus Insecticide Phosmet and Recombinant Mouse PrP and its Implication in the BSE Epidemic
I. Shaw1, C. Berry2, E. Lane1, P. Fitzmaurice1, D. Clarke3 and A. Holden1

(1) Centre for Toxicology, University of Central Lancashire, Preston, UK
(2) Department of Morbid Anatomy, The Royal London Hospital, London, UK
(3) CLRC Daresbury Laboratory, Warrington, UK


Abstract It has been suggested that exposure of cattle to the ectoparasiticide Phosmet in the 1980s caused a conformational change in the cellular prion protein (PrPC) to form the BSE prion (PrPSC), which initiated the epidemic of bovine spongiform encephalopathy (BSE).
Recombinant mouse cellular prion (r[mouse]PrPC) was exposed to the organophosphorus pesticide Phosmet in vitro and the conformation of the prion before and after exposure was monitored using circular dichroism (CD) spectroscopy, utilizing synchrotron radiation at the Council for the Central Laboratory of the Research Councils (CLRC) facilities at Daresbury, UK. Metabolites of Phosmet, generated in situ by rat microsomes, were investigated in the same way, to determine whether they might initiate the conformational change due to their high chemical reactivity.
Our studies showed that exposure of r[mouse]PrPC to Phosmet or microsomes-generated metabolites of Phosmet did not result in the conformational change in the protein from -helix to -pleated sheet that is characteristic of the PrPC to PrPSC conversion and, therefore, Phosmet is very unlikely to have initiated the BSE epidemic by a simple direct mechanism of conformational change in the prion protein.
bovine spongiform encephalopathy - circular dichroism spectroscopy - insecticide - organophosphate - Phosmet - prion - protein conformation



http://www.springerlink.com/(bmbpjj55ksv02p2wiismj555)/app/home/contribution.asp?referrer=parent&backto=issue,3,9;journal,31,74;linkingpublicationresults,1:103009,1



transmission studies do not lie, amplification and transmission!


i see NO properties of high levels of Manganese in the diet, combined with low levels of copper, in any of these primate
transmission studies.

1: J Infect Dis 1980 Aug;142(2):205-8


Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of
sheep and goats were transmitted to squirrel monkeys (Saimiri
sciureus) that were exposed to the infectious agents only by their
nonforced consumption of known infectious tissues. The asymptomatic
incubation period in the one monkey exposed to the virus of kuru was
36 months; that in the two monkeys exposed to the virus of
Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and
that in the two monkeys exposed to the virus of scrapie was 25 and
32 months, respectively. Careful physical examination of the buccal
cavities of all of the monkeys failed to reveal signs or oral
lesions. One additional monkey similarly exposed to kuru has
remained asymptomatic during the 39 months that it has been under
observation.

PMID: 6997404

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract


TSS
 

Kathy

Well-known member
Econo wrote:

Kathy, while you and flounder argue over the exact cause, it seems to me that in both cases the spreading of tses happens through the feeding of infected mamilian tissue. Is this correct?

Change the words: "infectious mammalian tissue"

to

"contaminated mammalian tissue"

and you are partially correct.

However, since there is now an abundance of cases, in Canada and elsewhere like the UK, where animals have developed BSE (and CWD) when they did not consume "contaminated" mammalian tissue - what caused it?

If you believe the likes of flounder, then you will forever live under the illusion that prion diseases cannot happen spontaneously due to environmental factors. If this is the pill you choose to swallow... then have a nice life, and don't ask any questions ever again....about anything. (Econo, I am being a little facetious here, don't take this personally!)Reality is merely one's state of mind. Do you live in the Matrix, or do
you see things as they truly are?

If you believe, as I do, that the occurrence of many diseases, including BSE, are the result of contamination of our environment and the subsequent bio-accummulation of metals, chemicals, and radio-active materials, then I will gladly share my thoughts and opinions with you econo. As for flounder (TSS)... I am not on this message board to convince him of anything. I could care less, if he listens to anything I say. He is free to believe whatever he wishes to.

There is an interesting article written by Dr. Murray Brian McBride, called "Prion Diseases and the Environment".
Link: http://72.14.203.104/search?q=cache:yEXED3kNHh8J:www.murraymcbride.com/TSE_Review03.pdf+%22MB+McBride%22+trace+metals+BSE&hl=en&gl=ca&ct=clnk&cd=1

I have communicated with Dr. McBride about why an earlier article of his did not reference Mark Purdey or Dr. David Brown's work(s). He stated that at the time he posted the article on the internet, he was not aware of their findings/hypotheses. Yet, his own hypothesis was/is very similar.

His follow-up paper (see link) does reference them. When I re-examined it, I realized that even Dr. McBride had found interest in Dr. A. Hamir's research on lead toxicosis in dogs (1984), as well as similarities to PEM (polioencephalomalacia). Both of these referenced papers made more of an impression on me, after I had re-discovered them on my own. I hope you will take a look at what Dr. MB McBride of Cornell University has to say.
 

Econ101

Well-known member
Kathy, I really don't know enough about this issue to really make medical research judgements. It seems to me that you or flounder could be right and that end result is the same. BSE is still being used as an economic tool by those influencing decision makers and the definitive studies on BSE are not being given enough resources. It allows the abuse of the issue to continue.

Japan is not taking U.S. beef becasuse of BSE and USDA goof ups. Japan is taking beef from Canada while the USDA does not allow the kind of testing Japan wants as assurance. I think Mike Callicrate's article puts it into the perspective of the market concentration game.

Whoever is right about the cause doesn't matter in this regard. The transmission and possible amplification is the problem. I am not willing to willy nilly trust the beef industry on this one as they have self interests all over the place and waiting for "proof" as some put it, could be too late to stop the transmission and amplification problem as it relates to human health.
 

Kathy

Well-known member
Econo,

There is no proof that BSE has caused human illness.

IF this FACT doesn't matter, then what the heck does?

Amplification and transmission cannot be resolved without first knowing the cause and what is being transmitted. Denying the involvement of trace metal imbalance or contamination will only perpetuate the suffering of all the ranchers trying to stay alive on their land.

If cause doesn't matter, reality doesn't matter!

You don't have to figure it out yourself, but everyone must put pressure on governments and research fund providers to look for the true agent. Proteins are not infectious.
 

Kathy

Well-known member
Dr McBrides final paragraph:

"
It now remains to be demonstrated whether TSE diseases are actually caused by a proliferation of self-replicating “rogue” prions, as is currently hypothesized, or whether certain pre-disposing factors such as Cu deficit or excess heavy metals alter prion formand function. If the latter is correct, then the prion deposits in diseased brain tissue could be a consequence or symptom, not a cause, of TSE diseases. It is now accepted that spontaneous TSEs, with no apparent source of infection, can arise . It would seemfeasible, then, that the BSE epidemic in the UK was a spontaneous TSE initiated by the changes in trace element or toxic metal bioavailability to marginally copper-deficient cattle. The fact that BSE appears to be transmissible to experimental animals does not rule out the nutritional origin, as there is now evidence that the protease-resistant (disease) form of the prion can be generated by metal displacement at binding sites of normal PrP, in the complete absence of the disease PrP. "

When McBride mentioned that foreign myelin injection experiments also caused paralysis and spongiform of the brain tissue, this really caught my attention. The resulting symptoms are similar to multiple sclerosis! Don't you think this deserves more investigation?

"
Injecting myelin protein into experimental animals causes animal paralysis and spongiform brain (Ebringer et al., 1997) which puts into question the animal transmission studies of BSE and other TSE’s that directly inject brain tissue from a diseased animal into the brain of another. Note that “control” animals are often injected with saline
solution, not uninfected brain tissue ). It has long been known, as explained by Root-Bernstein (1993), that the injection of foreign myelin tissue into experimental animals produces a disease referred to as experimental allergic encephalomyelitis (EAE), a disease that mimics multiple sclerosis in humans. It is also known that injecting pituitary gland extracts taken from cadavers into children suffering from dwarfism led to numerous human cases of iatrogenic CJD, even though no CJD “agent” was detected in the extracts( Rhodes, 1997). Other cases of iatrogenic CJD are reported to have resulted from the transplantation of other human tissues. An outbreak of iatrogenic scrapie in sheep and goats in Italy resulting from vaccination with vaccines containing animal tissue (Caramelli et al., 2001). Imperfectly purified extracts from tissues contain foreign proteins which can initiate autoimmune disease when injected into animals and humans."
 

Kathy

Well-known member
MUST READ REVIEW on PRION Science (2003) important points which are rarely covered.

"Prion Diseases and the Environment". by Dr. Murray Brian McBride, Cornell University, New York USA

Link: http://72.14.203.104/search?q=cache:yEXED3kNHh8J:www.murraymcbride.com/TSE_Review03.pdf+%22MB+McBride%22+trace+metals+BSE&hl=en&gl=ca&ct=clnk&cd=1
 

Kathy

Well-known member
Econo you stated to flounder in another thread:

It is amazing what you learn when you want to and you actually investigate.

How come when it comes to BSE and metal contamination all you can say is its political?

You need to head your own words. Why don't you actually read the Dr. MB McBride article, before, you fall-back on the "there is nothing we can do about it, it's political" BS.
 

Econ101

Well-known member
Kathy said:
Econo,

There is no proof that BSE has caused human illness.

IF this FACT doesn't matter, then what the heck does?

Amplification and transmission cannot be resolved without first knowing the cause and what is being transmitted. Denying the involvement of trace metal imbalance or contamination will only perpetuate the suffering of all the ranchers trying to stay alive on their land.

If cause doesn't matter, reality doesn't matter!

You don't have to figure it out yourself, but everyone must put pressure on governments and research fund providers to look for the true agent. Proteins are not infectious.

I think a good experiment with those scientists who believe this to be the case might prove your point. There might be a use for all those bse positive cattle after all. :wink:

If when you stop feeding ruminants to ruminants and then you get less cases of bse (as in brittain) in cattle then there has to be a link with that transmission route. The species barrier may be a barrier, but as we all know, genetically we are all a little different. flounder has already posted where the species barrier is not a barrier. The exposure to such contaminated material--whether it is what you or flounder says is the cause--is just a roulette game.

Some have already personally lost that game and want it stopped completely. I understand their point.

If it turns out that we sporadic bse is just a fact of life and we can't prevent it, well we will just have to deal with that. If it turns out that it could be stopped by amplifying infected ruminant parts, then the packers just have to deal with that. Lives are worth more than money---even if it is Tyson's money and they comparative advantage they sought by buying IBP.
 

RoperAB

Well-known member
On 770AM about three years ago on the David Rutherford show they had some kind of an expert from the UK that was basically saying the same thing about how BSE is going to occur naturally in a certain percentage of catle<really small percent>
They also claimed there was nothing new about BSE only that years ago people did not know what it was<called it the wobbles>
They also kept compareing it to cronic wasteing disease that wildlife get.
They also figgured that feeding animals back animal by products contributed greatly to BSE.
They also said if the meat was prepared properly it was still safe to eat.
I do know that the American Fish and Game who culls wildlife because of cronic wasteing says that the hunters can eat the meat of the culled deer and that as long as the meat is prepared properly its safe to eat.
Honestly I would not knowingly eat or feed to anybody a BSE animal or a deer with cronic wasteing disease. But my family has continued to eat beef<mostly hamburger>.
I think the risk is so low in North American of anybody getting sick from beef that I cant believe its such a big issue.
And yes I think its mostly political.
 

Econ101

Well-known member
RoperAB said:
On 770AM about three years ago on the David Rutherford show they had some kind of an expert from the UK that was basically saying the same thing about how BSE is going to occur naturally in a certain percentage of catle<really small percent>
They also claimed there was nothing new about BSE only that years ago people did not know what it was<called it the wobbles>
They also kept compareing it to cronic wasteing disease that wildlife get.
They also figgured that feeding animals back animal by products contributed greatly to BSE.
They also said if the meat was prepared properly it was still safe to eat.
I do know that the American Fish and Game who culls wildlife because of cronic wasteing says that the hunters can eat the meat of the culled deer and that as long as the meat is prepared properly its safe to eat.
Honestly I would not knowingly eat or feed to anybody a BSE animal or a deer with cronic wasteing disease. But my family has continued to eat beef<mostly hamburger>.
I think the risk is so low in North American of anybody getting sick from beef that I cant believe its such a big issue.
And yes I think its mostly political.

It is an issue to Japan. That alone, whether you are right or not about the safety of eating chronic wasting diseased animals or bse positives, should be enough to develop good policy over it. As Mike C. illustrated, the packers are using it gain comparative advantage in the industry. If you don't have packing plants in Canada and the U.S., where the policy is quite different, you are at a comparative disadvantage when it comes to competition. Bigger is better, not because it is more "efficient" but because size allows you to gain international comparative advantage. This will reduce the amount that producers get to a worldwide commodity price, with the costs that are extraneous to production not counted (environmental, labor, market rules, etc...) and everyone brought down to the lowest common denominator. Barriers to entry will be strategically employed to reduce competition (it has already happened in poultry).

We are setting up a world of oligarchs.
 

DiamondSCattleCo

Well-known member
Econ101 said:
Kathy said:
If when you stop feeding ruminants to ruminants and then you get less cases of bse (as in brittain) in cattle then there has to be a link with that transmission route.

<snip>

If it turns out that we sporadic bse is just a fact of life and we can't prevent it, well we will just have to deal with that. If it turns out that it could be stopped by amplifying infected ruminant parts, then the packers just have to deal with that.

I have by no means done anywhere near as much research on the topic as Kathy and Flounder, however I think we're going to find that BSE can be started through some combination of environmental factors much the same as CWD in elk. After all, we have 3 post feed ban positives up here, and I doubt there was feed left from 4 years earlier. Its definitely possible that it came from a blood based milk replacer.

However I think the evidence of transmission through feeding infected tissues is pretty overwhelming.

So why can't it be both? Sporadic starts by environmental conditions and/or injections, but transmitted and amplified by feeding ruminant remains? I do agree with Kathy that we need more time, effort, energy and money put into the causes of BSE, as well as solid proof of transmission before we can truly get a handle on it.

Rod
 

RoperAB

Well-known member
Econ101 said:
RoperAB said:
On 770AM about three years ago on the David Rutherford show they had some kind of an expert from the UK that was basically saying the same thing about how BSE is going to occur naturally in a certain percentage of catle<really small percent>
They also claimed there was nothing new about BSE only that years ago people did not know what it was<called it the wobbles>
They also kept compareing it to cronic wasteing disease that wildlife get.
They also figgured that feeding animals back animal by products contributed greatly to BSE.
They also said if the meat was prepared properly it was still safe to eat.
I do know that the American Fish and Game who culls wildlife because of cronic wasteing says that the hunters can eat the meat of the culled deer and that as long as the meat is prepared properly its safe to eat.
Honestly I would not knowingly eat or feed to anybody a BSE animal or a deer with cronic wasteing disease. But my family has continued to eat beef<mostly hamburger>.
I think the risk is so low in North American of anybody getting sick from beef that I cant believe its such a big issue.
And yes I think its mostly political.

It is an issue to Japan. That alone, whether you are right or not about the safety of eating chronic wasting diseased animals or bse positives, should be enough to develop good policy over it. As Mike C. illustrated, the packers are using it gain comparative advantage in the industry. If you don't have packing plants in Canada and the U.S., where the policy is quite different, you are at a comparative disadvantage when it comes to competition. Bigger is better, not because it is more "efficient" but because size allows you to gain international comparative advantage. This will reduce the amount that producers get to a worldwide commodity price, with the costs that are extraneous to production not counted (environmental, labor, market rules, etc...) and everyone brought down to the lowest common denominator. Barriers to entry will be strategically employed to reduce competition (it has already happened in poultry).

We are setting up a world of oligarchs.

I understand what you are saying,but I think many in the beef industry have the wrong attitude.
I get the impression that people in the industry look at it like a pie. Example there are only so many pieces of the pie to go around. If we can start a negative ad campain we can take somebody elses <another beef producers> piece of the pie.
Im thinking if there is a pie its not just limited to current customers that purchase a set amount of beef.
Im thinking if beef producers worked together in a positive way that we could expand the market and all beef producers would be better off.
Together would should be promoteing beef over other forms of protien. Maybe get people to eat beef instead of stuff like pasta. Look for ways to make it more affordable at the retail level instead of looking for ways to drive up the retail cost of beef that would not putany more money in the pockets of producers such as manditory country of origin labeling.
Wealth is created/ there is no set amount
 

Econ101

Well-known member
DiamondSCattleCo said:
Econ101 said:
Kathy said:
If when you stop feeding ruminants to ruminants and then you get less cases of bse (as in brittain) in cattle then there has to be a link with that transmission route.

<snip>

If it turns out that we sporadic bse is just a fact of life and we can't prevent it, well we will just have to deal with that. If it turns out that it could be stopped by amplifying infected ruminant parts, then the packers just have to deal with that.

I have by no means done anywhere near as much research on the topic as Kathy and Flounder, however I think we're going to find that BSE can be started through some combination of environmental factors much the same as CWD in elk. After all, we have 3 post feed ban positives up here, and I doubt there was feed left from 4 years earlier. Its definitely possible that it came from a blood based milk replacer.

However I think the evidence of transmission through feeding infected tissues is pretty overwhelming.

So why can't it be both? Sporadic starts by environmental conditions and/or injections, but transmitted and amplified by feeding ruminant remains? I do agree with Kathy that we need more time, effort, energy and money put into the causes of BSE, as well as solid proof of transmission before we can truly get a handle on it.

Rod

Whatever it is, I want to take the power over political decisions about it out of the hands of paid off politicians who are advocating obvious packer policies against producers and other competitor packers.

You don't have a market if you don't have competition.
 

DiamondSCattleCo

Well-known member
Econ101 said:
Whatever it is, I want to take the power over political decisions about it out of the hands of paid off politicians who are advocating obvious packer policies against producers and other competitor packers.

Certainly. Thats why I advocate more and more dollars being spent to BSE research. The sooner we are able to discover the scientific truth about the causes and the transmission of the disease, the sooner we can squelch the closed borders and the packer's abilities to profit from those closed borders.

Rod
 

flounder

Well-known member
ECON WROTE ;

If when you stop feeding ruminants to ruminants and then you get less cases of bse (as in brittain) in cattle then there has to be a link with that transmission route. The species barrier may be a barrier, but as we all know, genetically we are all a little different. flounder has already posted where the species barrier is not a barrier. The exposure to such contaminated material--whether it is what you or flounder says is the cause--is just a roulette game. ............


AMEN!, and by the numbers ;


10. Mr Patrick Burke (Defra) presented epidemiological data on BSE

cases in the GB cattle herd, and of cases in other countries, and

summarised the surveillance undertaken in the UK. The GB BSE

epidemic peaked in 1992 with over 36,000 cases confirmed. This

has since been in steep decline with 203 cases confirmed in 2005

and only a few (n=18) confirmed cases so far in 2006. The

average age of onset of clinical BSE has increased with time. The

proportion of clinical suspect cases subsequently confirmed as

BSE has declined, probably due to the reduction in number of BSE

infected cattle in relation to the number with other diseases. The

incidence of GB BSE cases born after the 1996 reinforced feed

ban (BARB cases) was also in decline. To date, 124 GB BARB

cases had been identified.


snip...



http://www.seac.gov.uk/minutes/draft-91.pdf



i see no metals or ops in the formula of this decline, only tainted feed i.e. infectious transmission, maybe kathy can explain this :lol2: :lol2: :lol2:


TSS
 

Econ101

Well-known member
RoperAB said:
Econ101 said:
RoperAB said:
On 770AM about three years ago on the David Rutherford show they had some kind of an expert from the UK that was basically saying the same thing about how BSE is going to occur naturally in a certain percentage of catle<really small percent>
They also claimed there was nothing new about BSE only that years ago people did not know what it was<called it the wobbles>
They also kept compareing it to cronic wasteing disease that wildlife get.
They also figgured that feeding animals back animal by products contributed greatly to BSE.
They also said if the meat was prepared properly it was still safe to eat.
I do know that the American Fish and Game who culls wildlife because of cronic wasteing says that the hunters can eat the meat of the culled deer and that as long as the meat is prepared properly its safe to eat.
Honestly I would not knowingly eat or feed to anybody a BSE animal or a deer with cronic wasteing disease. But my family has continued to eat beef<mostly hamburger>.
I think the risk is so low in North American of anybody getting sick from beef that I cant believe its such a big issue.
And yes I think its mostly political.

It is an issue to Japan. That alone, whether you are right or not about the safety of eating chronic wasting diseased animals or bse positives, should be enough to develop good policy over it. As Mike C. illustrated, the packers are using it gain comparative advantage in the industry. If you don't have packing plants in Canada and the U.S., where the policy is quite different, you are at a comparative disadvantage when it comes to competition. Bigger is better, not because it is more "efficient" but because size allows you to gain international comparative advantage. This will reduce the amount that producers get to a worldwide commodity price, with the costs that are extraneous to production not counted (environmental, labor, market rules, etc...) and everyone brought down to the lowest common denominator. Barriers to entry will be strategically employed to reduce competition (it has already happened in poultry).

We are setting up a world of oligarchs.

I understand what you are saying,but I think many in the beef industry have the wrong attitude.
I get the impression that people in the industry look at it like a pie. Example there are only so many pieces of the pie to go around. If we can start a negative ad campain we can take somebody elses <another beef producers> piece of the pie.
Im thinking if there is a pie its not just limited to current customers that purchase a set amount of beef.
Im thinking if beef producers worked together in a positive way that we could expand the market and all beef producers would be better off.
Together would should be promoteing beef over other forms of protien. Maybe get people to eat beef instead of stuff like pasta. Look for ways to make it more affordable at the retail level instead of looking for ways to drive up the retail cost of beef that would not putany more money in the pockets of producers such as manditory country of origin labeling.
Wealth is created/ there is no set amount

Roper, I think Canadian beef would go well with a lot of consumers. Your fears of labeling are being played on here. It should be an asset and a marketing bonanza if you produce higher quality meat.

When consumers can't tell if their meat is coming from a specific country, or what the grade is because it is not labeled, they can not make decisions as to what differences in quality make a difference to their family before the purchase. It also globalizes the meat business and brings the cost of meat down to the world market price and world market qualtity.

I did go buy some of that ground beef from Walmart that was at a really low price. It did taste different. Each of the extrusions was a little tougher and it cooked up a little different than any other kind of ground beef I have had before. I will pay a little more for the quality of ground beef we are used to. How will I know that is the case if I can't tell the meat comes from Canada or the USA? How will I be able to compare?

I know the category is huge, and ground beef is different than steak, but if my shirt is labeled as to country of origin, why shouldn't what I eat be labeled?

I for one would look for some of those advertised Canadian cuts just to see if you guys were telling the truth about it. If it was produced by a smaller packer and labeld as such, I would also be more inclined to buy it.
 
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