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Fears grow over 'mad elk disease'


19:00 02 April 03

Exclusive from New Scientist Print Edition

The death of three hunters from Creutzfeldt-Jakob disease is likely to heighten fears that people in North America are contracting a new form of the fatal brain disorder from deer. But the surveillance system in the US is so woefully inadequate that even if these fears are unfounded, it is impossible for researchers to rule out the possibility.

Chronic wasting disease (CWD) is a prion disease spreading among elk and mule deer in North America. It is similar to mad cow disease, raising fears people eating contaminated venison could develop a form of Creutzfeldt-Jakob disease (CJD) like that blamed on contaminated beef, which has killed about 200 people in Britain.

This is why the latest cases of CJD in hunters, to be reported at the American Academy of Neurology's meeting in Honolulu this week, are causing concern. Two of the men, one aged 64 from Washington state and the other aged 54 from Alaska, were treated by neurologists Natalia Murinova and Ali Samii at the Seattle VA hospital.

"These two cases may well have no relationship to CWD in elk and deer," says Samii. "But the fact that it happened in these two patients brings up that question." The third man died in a different hospital but was from the same town as the hunter from Washington. The two were friends and hunted together.

Disease-free state

However, the Centers for Disease Control and Prevention (CDC) will not be investigating the cases because there is no evidence that the men ate CWD-infected meat, says spokesman Ermias Belay.

So far the CDC has only investigated CJD cases from states where deer are known to have the disease. But Washington and Alaska are not necessarily disease-free: states do not have to test for CWD until the disease is known to be present.

The CDC has investigated a few suspect CJD cases in the past, and found no compelling evidence of CWD transmission to humans. However, "the data seeking such evidence are very limited", Belay admits.

And that is because not many doctors are looking. For example, Pierluigi Gambetti of the National Prion Disease Pathology Surveillance Center in Cleveland, Ohio, has found that between 1997 and 2002 about 60 per cent of the 921 suspect cases were confirmed as being a prion disease.

But these cases amount to fewer than a third of the number that would be expected for the same period based on the rates of sporadic and familial CJD elsewhere, he will tell the Honolulu meeting this week.

No guidelines

That shows how ineffective the surveillance is, says Norman Foster, a neurologist at the University of Michigan in Ann Arbor. So if CWD-contaminated venison does trigger a new form of CJD in people, there could be dozens of extra cases of CJD without them being detected.

Part of the problem is that CJD resembles common diseases such as dementia in the elderly. Doctors have no set guidelines on what to look for and only autopsies can confirm a diagnosis. But few are carried out and CJD is not a reportable disease in the US.

Autopsies can also distinguish between sporadic CJD and the variant form triggered by mad cow disease. But since no one knows what the brains of people with "CWD-CJD" would look like - if the disease does indeed exist - it is hard for pathologists to be sure that a particular CJD case is not related to CWD.

To compound matters further, different federal agencies are responsible for surveillance in humans and animals. Foster and others are pushing for a surveillance programme similar to Britain's mad cow disease and CJD surveillance programmes.


Anil Ananthaswamy

DeafDog,
To be on the safe side, I serve "new meat" to the In-Laws, as a trial run, prior to use by the immediate family. Unfortunately, no problems, this far.

That piece of info is actually outdated. I believe two of the three cases are now thought to be NOT have been Creutzfeld-Jakob.

A good place to start for background is at cwd-info.org.

At this time, research shows that CWD does NOT jump the species barrier to either cattle or humans, and the disease is still quite localized, with only a few "small" areas infected.

I wonder if it jumps the species barrier to wolves? Dutch.

That looks like a bunch of convoluted clap trap by some one looking to get a big government grant to research it. It says alot, without saying anything, and reaches no conclusion, except to say that they may be wrong.

Cook your meat well. Even healthy deer and elk can carry many parasites in the flesh.

Dutch is right. That was proven false. I eat the meat. The media has blown this way out. Lots of speculation but few facts. It has not been found outside of any non deer animal.

Yes, venison is safe to eat. I think to be on the safe side I would avoid eating nervous sytem tissue (brains, spinal chord etc.) and avoid contact of these tissues with other cuts of meat from the animal. Just because something has yet to jump the species barrier, doesn't mean you wont be the unlucky bastard who gets it first! Just ask those poor english guys who got the wierd ass variation of mad cow.

JMHO,

JohnTheGreek

JohnTheGreek

Thanks for the reminder. It makes me feel sick. Are you absolutely sure that you are not working for the helth department

I have quited eating sausages since you never know what they are containing, brains, tissue, or other sleezy stuff ???

I have to stick more to Kosher from now on

Cheers
/ JOHAN

I think eating nervous system tissue or brains is not that difficult to give up. Especially if you have to back pack it out 3 miles...... lol! Just remember to cut the horns off last.... Dutch.

The stories that go around and around about CWD and CvJD, and Mad Cow are never ending. Most of the story was disputed and found to be incorrect. Of the hunters who have contracted CvJD, they had been in Europe and consumed meat that was thought to be suspect. CWD had no bearing on it.

However, it is still wise to be responsible about consuming venison from those areas that may have CWD. Mind the nervous tissue and consider having the critter tested before consuming the meat. Its not that expensive, and it doesn't take much time.

Read on, for those who are not afraid.
The WASTING LANDS - the CWD epidemic in deer
by Mark Purdey

Chronic Wasting Disease of deer is much the same as scrapie in sheep. It is a traditional variant of the spongiform encephalopathy (TSE) range of diseases; a previously unheard of neurodegenerative syndrome made famous by the outbreak of mad cow disease in the UK .

Seven per cent of the free ranging/captive deer and elk population residing along a 100 mile length of the Front Range of the Rocky Mountains in North Colorado and South East Wyoming have been affected with this disease for several years now. Originally identified as a TSE in the late 1970's by veterinary neuropathologist, Professor Beth Williams, the disease could have been endemic for many decades. Any rancher or hunter who had noticed these ailing deer hobbling around the place, had probably put such cases down to premature ageing or some �weakling� wasting condition.

The origins of hyper infectious hysteria.

Despite the long term tradition of CWD haunting the Front Range foothills, a surge of near hysteria has bestruck the official US wildlife departments whose job it is to preside over CWD. Following in the footsteps of the official furor over mad cow disease in Europe, the US government has sadly adopted the same unproven hypothetical mindset on the origins of these diseases; that TSEs stem from exposure to hyper infectious �prions� that are readily transmitted via body to body contact (saliva, etc), or via �prion� contaminated feed. In this respect, blame has been conveniently offloaded onto the deer themselves � for sharing the same feed troughs, etc, � or onto the hunters for transporting the �infectious� agent around with them from shooting region to region.

But why has such a deeply flawed and scientifically inept theoretical consensus been permitted �gospel� status for such an unusually protracted period of time? The launch of any new theory into the notoriously sceptical scientific establishment invariably attracts a fair degree of healthy challenge. But strangely enough with TSEs, there has been an exception to this rule. This is largely because the UK government has been actively engaged in tailoring or outright suppressing, any publicity surrounding dissident scientific studies that invalidate or even begin to threaten any aspect of the official hypothesis. Furthermore, it is strange to witness the same old �masters of complacency� in the higher echelons of UK officialdom, suddenly adopting a high degree of hypersensitivity over the way that they deal with their affairs. Such an incongruous style of official behaviour has betrayed a deep level of insecurity over anything that they are telling us on BSE.

For instance, nobody has been told that the British meat and bone meal (MBM) feed that was held responsible for the massive BSE epidemic in the UK has been exported by the cargo boat load, to cattle herds all over the world since the 1960s - yet the majority of those countries have never suffered a single case of BSE in their cattle herds to date. Nor does anyone know about the 40,000 cases of BSE that have appeared in UK cows that were born after the 1988 ban on MBM going into UK cattle feed. In this respect, nearly a quarter of the total cases of BSE in Britain cannot be explained by the conventional causal theory! In some BSE endemic countries, more than half of their total BSE cases were born after their respective MBM bans. Even my five year old son can see the stupidity of such an obvious �cover story�.

To escape the embarrassment of the outright failure of control measures, the UK government set about hoodwinking the British public and their foreign interests by creating a second feed ban in 1996; whereupon they instructed their spin doctor journalists to misappropriate blame for the unaccountable 40,000 cases of BSE onto �leakage of micro amounts of MBM left over in the feed silos getting into cattle feed�. They then gave full coverage to the fact that the government were now banning the inclusion of MBM going into feeds destined for all types of farm livestock. The 1988 ban was subsequently forgotten and conveniently erased from the public memory banks. But today, 22 cases of BSE have now emerged that were born after this second 1996 ban!

This whole hyper infectious myth has been based on the fact that TSEs can be transmitted in the laboratory; whereby TSE affected brain tissue is injected into misfortunate laboratory animals that subsequently contract TSE. The fact that classes of Alzheimer�s and other neurodegenerative diseases can be transmitted in this way is completely ignored. But these transmission experiments prove nothing in terms of demonstrating whether TSEs are caused by a microbiological infectious agent or not. After all TSEs do not fulfil Koch�s postulates; the conventional yardstick for assessing whether a given disease stems from infectious origins.

The �all important� success of these �trumped up� transmission experiments could have equally easily represented the fact that a highly toxic chemical or metal species which had originally contaminated and killed the initial TSE diseased animal was then being transmitted into a secondary host. Once again, this equally feasible alternative explanation has been ignored.

But one of the first lines of epidemiological inquiry aimed at investigating the origins of CWD ought to have addressed the question why the disease has not spread like wildfire, wiping out susceptible individuals of the deer population residing right across the entire Rocky mountain ranges. But whenever the likes of rancher and hunting folk who live and breathe with the deer has attempted to infiltrate the CWD debate, their intuitive and practical perspectives on the disease have invariably been rebuffed by the official and scientific policy makers.

Historical truths ignored.

A global study of the most basic rudiments of the history of TSEs clearly demonstrates that this disease does NOT spread via animal to animal contact or via ingestion of the �infected� by the �uninfected�. For instance, when I was researching the most intensive global hotspot of sheep scrapie in the northernmost Icelandic fjords, I found that the Icelandic sheep farmers had adopted the custom of slaughtering any sheep the moment the first symptoms of scrapie emerged. This tradition had not evolved from any fear of the disease exploding in the sheep population - since scrapie has occurred at a consistent incidence rate for light years in Iceland � but was carried out because the hard pressed farmers thought it best to eat the sheep (brains and all!) before the wasting symptoms of scrapie reduced the poor beast to skin and bones.

So if scrapie or CWD can be passed onto humans via consumption - as the scientific authorities would have us believe - why have no cases of CJD erupted in these Icelandic sheep farmers? In fact, Iceland has only ever witnessed two cases of CJD in its entire medical history, and these victims had both hailed from the scrapie-free district in the far south of the country.

A historical study of official government attempts to control both scrapie in Iceland and CWD in Colorado reveals the repeated FAILURE of several wholesale slaughter programmes that were executed in these well renowned, long standing TSE hotspot areas. After the deer and sheep had been culled across the vast tracts of land implicated in these TSE endemic regions, the fresh livestock introduced after a four year fallow period simply started to go down with the disease all over again.

Disturbingly, it seems that the US authorities have failed to learn such a simple lesson, and are following the farcical footsteps of their European counterparts, channelling public funds back into renewed slaughter schemes in Colorado and Wisconsin � schemes that are ironically no different from those which have already failed!

The repeated failure of these trials clearly indicates that the cause of this disease lies in the particular ENVIRONMENT where these animals were pastured. The answer must lie with some specific idiosyncratic factors commonly shared by all of the ecosystems where these spongiform hotspots erupt. An analytical field study of these regions provided a golden opportunity to pinpoint the aetiological needle in the causal haystack.

Low Copper ; the primary environmental prerequisite of TSE ?

As part of my eco-detective treks visiting isolated TSE clusters all over the world, I came to research CWD in Colorado in the early 1990s. I soon realised that if the deer had been roaming those canyons for long enough, CWD would be as old as the pre Cambrian hills that towered above me. I drew a criss-cross of soil samples right across the CWD endemic area, and I remember the flecks of mica and schist that caught the razor-sun rays, almost dazzling me a few times � a phenomena that I had become well accustomed to during my sampling sprees in so many regions around the world; intensive sunlight, and more importantly, these specific geo-elements which characterised the granite terrain that underpinned every single long standing TSE cluster zone that I had visited to date. Furthermore, this observation virtually guaranteed that my environmental analyses would, once again, come back �zero copper� from the lab � the causal cornerstone of spongiform disease pathogenesis.

I was also intrigued to learn that the only spongiform susceptible species which had failed to go down with the disease in the CWD endemic area was the pronghorn antelope � an indigenous antelope that is well adapted to its centuries old occupation of Rocky Mountain terrain. The Pronghorn can conserve levels of copper and selenium in its body considerably more efficiently than any other species of cervidae. Perhaps its metabolic predisposition for copper conservation which the other species do not possess explains why the pronghorn has resisted CWD?

In this respect, it was of no surprise when I heard the recent news that CWD had now been identified in deer living around Mt Horeb in Wisconsin � another copper deficient granite stronghold that has withstood the erosive elements over time. But for how long has CWD been around in Wisconsin? The disease may have been there for years, but only just been identified because of the recent surge of political sensitivity and scientific intrigue surrounding this disease; thereby raising the �CWD awareness� profile sufficiently to recognise the disease. But if CWD has only just emerged, it has to be considered that copper deficiency has blighted these granite terrains for centuries and cannot therefore be held as solely accountable for the recent eruption of CWD.

Metal Detector.

An ideal research study presented itself after I located two Icelandic valleys fifteen miles apart; where one valley played host to sheep flocks which were riddled with scrapie, whereas the other valley supported sheep flocks which were entirely scrapie free. Intriguingly, sheep from both valleys had been freely intermixing on the open mountain during summertime - once again discrediting the conventional theory which assumes that scrapie transmits via animal to animal contact.

So the answer to the causal question clearly lay with some unusual combination of environmental factors that are present in the scrapie valley, yet absent in the scrapie free valley.

I ended up carrying out many self funded field analyses in Iceland and other TSE cluster regions in Japan, Slovakia, New Quinea, Colorado, Italy, Sardinia, etc. After many cul de sacs and false leads, I believe that my observations have actually now identified those common toxic denominators � low copper/high manganese combined with high intensities of low frequency infrasonic shock - the key factors which have subsequently been shown to produce the fully fledged prion in laboratory cell cultures - eg; the malformed prion protein which characterises the brains of all animals affected with spongiform disease.

In the Icelandic scrapie valley, the levels of copper in the pasture were rock bottom for natural reasons. Whereas the high levels of manganese had originated from volcanic emissions; with subsequent accumulation of manganese in the pasture grasses due to the characteristic wetness of the pastures in the scrapie valley - where the resulting soil acidity renders manganese freely available for uptake into the pasture grasses. The source of intensive infrasound in this valley specifically stems from the earthquakes and earth tremors that have consistently issued from the major tectonic fault line which runs past the head of the valley � the nearby town of Dalvik was flattened by one such earthquake in 1938.

I subsequently identified the same set of common toxic denominators in the Colorado CWD cluster area. My field survey and analyses revealed low copper throughout the deer�s food chain, in combination with a dietary �fetish� of the densely populated local deer for consuming large quantities of pine needles � which analysed out at 2000 + ppm of available manganese. Another more disturbing issue surrounding manganese intake stemmed from the fact that deer hunters were being sold minerals that were intended to addict deer to their hunting territory. In this respect, the hunters have been unwittingly shooting their own industry in the foot, by putting down these dual purpose minerals that have been formulated to addict deer to their shooting grounds as well as for forcing the sturdy growth of their antlers. Guess which mineral is added for forcing antler growth? My contacts from Wisconsin also report use of these manganese minerals in their CWD hotspot region.

Intriguingly, the CWD endemic region of Colorado is also well noted for its high intensities of natural radiations of low frequency infrasound. Not only does it lie along a major fault line that runs up the Front Range ridge � producing its fair share of mini earthquakes and tremors over the years � but several publications have highlighted the high intensities of infrasound that derive from the atmospheric turbulence and winds passing over the mountain ridges of this specific region. The large number of explosions from the intensive quarry blasting activities in this area should also be considered as relevant sources of artificial infrasound, just as the intensive testing of missiles down at Whitesands missile range in New Mexico and another testing range near Mt Horeb in Wisconsin may also serve as these relevant sources of artificial infrasound in these recently declared CWD outbreak regions.

Infrasonic shock waves, high manganese, low copper; what�s the connection with CWD ?

Whilst there seems to be a correlation between the presence of this package of environmental toxic denominators and the timing and distribution of CWD outbreaks in the USA, how can all of these factors prove relevant to the cause of these mystery spongiform lesions found in the brains of the victims of these diseases?.

An alteration in the normal molecular shape of a specific brain protein, known as the prion protein, has been shown to be a critical deciding factor in the development of TSEs; since a deformed prion protein hallmarks the brains of all those mammals who have died of TSEs, perhaps indicating that some loss of function of this protein is all part and parcel of the TSE disease process. Intriguingly, the prion protein has been shown to bond up with copper in the normal healthy brain, and I have hypothesised that the copper found attached to the prion protein plays a role in conducting the electromagnetic energy that is received from incoming sources of ultraviolet, geomagnetic, infrasonic radiations, etc, form the external environment. These energies are utilised for the bodies own balanced metabolism; for regulating circadian mediated functions such as immune defence, growth and repair of cells, sleep/wake cycles, etc.

But when copper is in short supply in the brain, due to certain environmental influences, the prion protein is capable of bonding onto certain alternative metals, such as manganese, bismuth or silver. But these foreign substitutes may not act in the overall best interests of the organism. For instance, manganese will store up electro energy instead of conducting it like copper; thereby blocking the flow of electromagnetic energy that is required for regulating certain vital body functions.

But one of the specific characteristics of manganese is that it can absorb the energy of sound � such as the high intensities of �phonon� energy that are insidiously radiated with the inaudible low frequency range of sound, known as infrasound. But manganese can only absorb this energy when found in its specific �trivalent� manganese form; whereupon the sound energy actually metamorphoses the atomic structure of the manganese so that it can become permanently magnetised. So whenever an individual who is carrying excessive levels of this freaky form of trivalent manganese in their brains enters into an external magnetic field, the manganese bonded prion proteins become permanently magnetised to explosive flash point levels; whereby self perpetuating, chain reactions of free radical mediated neurodegeneration burst forth, and TSE pathogenesis ensues.

Whilst high intensities of trivalent manganese may be �manufactured� in the living brain via an �oxidative transformation� of manganese 2+ in the retina by incoming ultraviolet radiation or other eco-oxidants, etc, it is also possible that an exclusive source of trivalent manganese has got into the food chains in TSE endemic areas; via its incorporation into animal feeds or mineral licks, etc, or via their natural presence in the indigenous geological bedrock of the TSE region. Such a scenario may explain why hunters who are feasting off deer shot in CWD regions who have thrived off mineral licks/pine needles containing trivalent manganese, will, in turn, become contaminated with trivalent manganese themselves; and thereafter rendered hyper susceptible to the low frequency infrasonic shocks in their hunting environment (eg; natural infrasound, rifle shots, etc ).The same eco-prerequisites that caused CWD in the deer are now primed and present in the human hunter. CJD could result.

Not only has this abnormal mineral imbalance been consistently identified in all of the ecosystems blighted by clusters of TSE, but studies on the brains of CJD casualties by Case Western University�s US Prion Disease Surveillance Unit have identified a 10 fold higher level of manganese and 50% reduction of copper in relation to control brains. Furthermore, Dr David Brown at Cambridge University in the UK has produced the TSE-like malformed prion protein in cell culture experiments after adding manganese to copper deprived cells.

Despite publication of all of these complementary field and laboratory studies in prestigious scientific journals, the various European health authorities and their key TSE advisors are blindly ignoring these findings. Not only are they discarding such an important fresh direction in TSE research, but they are doing their utmost to publicly marginalize those of us who are trying to pursue this line; and using public money to implement their tactics of suppression into the bargain!

The Genetic Connection.

Whilst it is true that all types of TSE require components of genetic susceptibility in their causal interplay, the TSE susceptible individual still very much requires the additional exposure to these toxic environmental factors before the disease can ever begin to manifest itself; Witness, the large number of scrapie susceptible sheep that live in scrapie-free Australia but never develop the outward symptoms of scrapie. Yet whenever Aussie sheep are exported to countries where scrapie is endemic, symptoms of scrapie invariably break out - presumably because the environmental causal factors are absent in their native Australian terrain, yet fully present in the importing countries.

The same scenario is duplicated in respect of a CJD susceptible Greek-Italian population that lives in many regions across southern Italy. But CJD has only ever erupted (at an excessive incidence rate) in just one of the many hamlets where these people live - a hamlet that is exclusively exposed to the specific environmental prerequisites that initiate TSE.

A multinational master plan ?

Since all of the evidence points to the fact that TSEs are caused by a clear cut combination of genetic and toxic environmental factors, why do the authorities worldwide continue to handle these diseases as if they stem from highly infectious origins?

I can only assume that the rigid adherence of Establishment bodies to the reductionist mindset - regardless of whatever new evidence comes to light - merely betrays the current global agenda to depopulate livestock numbers for reasons that have nothing whatsoever to do with health risks to the human race.

The true picture is one of a mere handful of politically-motivated, sociopathic pseudo scientists who predominate the upper echelons of the UK's and EU�s agricultural and scientific ministries. These incestuous �experts� are singing for their supper. They are on the pay role of the global corporations whose sole interest lies in forcing open a market place for their GM arable protein products. Powerful organisations who have no interest in making life easy for their competitors; eg; those of us who are trying to make a living out of selling livestock proteins.

We only have to ask ourselves who are the key culprits that are currently capitalising on the fashionable scare stories which maintain that �BSE prions will exterminate us all�? - the multinationals. Who is spinning out the propaganda myths that beef, lamb, venison, game and organic food (grown from animal manure) are contaminated with prions; and are therefore unfit for human consumption ? - the multinationals!

We must remain aware that these corporations have invested billions of bucks in researching and developing their GM arable protein crops and the complementary package of pesticides to go with them. They have bought up oceans of acres of dirt cheap arable land across Eastern Europe, the Third World and North/South America and they are clearly going to attempt to smash anyone competing for �their� protein market who gets in the way.

Despite the scare mongering, a basic study of the history of CWD clearly demonstrates that this disease does NOT originate from deer to deer contact. Despite such a simple observation, a manic mindset has recently gripped the whole US nation who have jumped to the assumption that this disease stems solely from hyper infectious origins. Any evidence put forward for an environmental cause has been blindly ignored. In this respect, the recent discovery of another cluster of CWD in Wisconsin has invoked an official overreaction of unprecedented proportion � a wholesale slaughter policy has been enacted throughout CWD endemic regions across the USA.

But who is questioning the scientific reasoning of the US authorities for executing their final farcical solution on these poor creatures? For this latest turn towards a unilateral policy of �totalitarian overkill� of a few thousand healthy deer has been received with almost complacent acceptance across the country. Such perverse and senseless 'carry-ons' have sadly become the daily 'non-stories' of our modern times � particularly here in Europe; where reports pop up with ever increasing frequency of so called TSE precautionary control programmes initiating slaughter regimes all over the globe - annihilation of a herd of water buffalo in Vancouver, flocks of sheep from Vermont, flocks of sheep in Sardinia, 1000�s of sheep flocks in Germany, 400,000 cows in Germany � all healthy animals. So what next ? The entire BSE-free British sheep flock on the grounds that BSE might just appear in British sheep?

The sad twist to this tale is that straightforward copper supplementation of deer in CWD risk areas may be all that is required to prevent manganese replacing the depleted copper at the critical prion protein bonding sites in the deer�s brain; which, in turn, prevents the �knock on� increase in susceptibility of the animal to environmental infrasound; that insidious eco-force to be reckoned with, capable of triggering off a melt down of self perpetuating, free radical �cluster bombs� in the brains of manganese contaminated deer, thereby instigating CWD. Furthermore, copper supplementation may be all that is required to prevent the senseless slaughter.

Mark Purdey - September 2002

--------------------------------------------------------------------------------

I had venison pan sausage for breakfast this morning. There is no major problem here. Where there have been outbreaks the various agencies involed are on top of it. There was, and continues to be a lot of media hype here (as with most things).

Bob

Here is a link to the National Wildlife Health Center. It is an excellent source to stay current.
NWHC Link

[ 04-04-2003, 18:31: Message edited by: Bob in TX ]

AKBman, it is illegal in the US, and has been since 1996, I believe, to feed meat and bone meal to any ruminant. This ban is actually being enforced (as opposed to hoodwinked at) by the FDA.

While the Europeans were hysterically trying to avoid our Starlink soybeans (genetically altered to resist Roundup), they were happily munching on head cheese made from BSE infected cattle.

Sometimes, irony is it's own reward.....LOL! Dutch.

Intresting article by Mark Purdy, but I have a couple of questions about his assumtions..
a) Why would the British Government and the British scientific community completely ignore this theory if there was any substance to it? Copper suppliments would have been a far cheaper course than the massive cull we had.
b) Why have the scientific communities from around the world not pulled the British up if they are so wrong?

BSE is still very much an issue in the UK in scientific circles. At the moment their two big fears are: a) That BSE can be transmitted from cow to calf via the milk and b) That BSE is present in the national sheep flock but has historically been misdiagnosed as scrappie. Either one of those scenarios would be another big blow to our farming industry.

Back to CWD in deer. I thought this had been traced back to deer or elk which had been kept at a research station where previously scrappie infected sheep had been grazed intensively for a number of years?

Purdey's article is very interesting. Of course the whole problem stems from not teaching science. Surveys have shown that most americans no nothing about even the basics of science. But hysteria rules , here in NY they will not permit hunters to bring venison in from states that have cwd. I thank Mr Purdey for puting a little light on the subject.

been eating venison almost exclusively since November. Maybe thats why I can't think straight?

I am not saying the theory presented is correct, but it does present a different angle. I think much of the hysteria surrounding CWD is being purported by the anit-hunting groups. What better way to get people to stop hunting than to use fear of the game animal itself. I also wonder if current high game populations and densities have anything to do with the situation. From the information I have found, 95% of the cases are in areas with fairly high population densities, the big hole in that theory is the South East where deer are thick as ticks on a coon hound, yet they seem to have escaped this dilema. I will still hunt deer when I return to New Mexico, and I will eat what I kill.

I eat a lot of venison, and I've eaten a lot from the areas that have CWD. IMHO Purdey's article makes as much sense as the prion hypothesis.

I'm of the opposite opinion: the copper theory is utter rubbish.

If it was a lack of copper, a simple addition of copper to the diet should either reverse or stop the progression of the disease. This is not the case.

If copper is the issue, why does CWD appear on game farms (where they use mineral blocks!!!!!), but not on the surrounding areas, until CWD shows up on the farms?

A few simple thought experiments is all that is needed to reject such this simplistic hypothesis. JMO, Dutch.

Guess what?, we have had CWD for a 100 years in the USA, we just didn't know it!! all these die offs in areas have been around as long as I have been around and that's a long time....I have been eating deer and elk for about 65 plus years, so far so good...I gave up antelope some 64 years ago, never regreted that decision...

Dutch,
in Redmond, Oregon there is a feed processing plant that grinds up meat & bone to add to livestock feed. I called them hoping that they were a dog food processing plant and sure enough it was for livestock use only and I could not think of any livestock in USA that eat meats naturally. Right now I'm trying to find out if Oregon Fish & Wildlife was or is a customer because if they are, then they are providing elk & deer with these meat & bone added livestock feeds in the wintering areas.

Norseman, there still is value in meat and bone meal. For example, we use it heavily in our fish feeds.

If they are using meat or bonemeal in ruminant feed, the FDA will be very interested to know about it.

Our fish feed manufacturer used some Canadian bone meal last year(?) that was tracked back to a CWD infected elk ranch. Talk about the feds being all over those poor guys....... No harm done (all of it went into trout feed), but a very interesting experience for all involved, nonetheless.

If bone meal is actually being used in ruminant feed, someone better expect a visit by the men in suits. I'm betting pigs or chickens, however. JMO, Dutch.

Don't cook it well, keep it rare. If you are worried, test it ($17 in Colorado, free if it is in a mandatory testing unit) then be assured that it is now safer than other untested meats you buy at the grocer.

Deke.

I make chili with deer at least once a week and have done so for years.I am quite healthy in fact more so than most people I know.I once took a pot of my chili to a superbowl party lots of liberal tree huggers were in attendance and loved my chili and then they enquired about the ingredients.A lot of them rolled there eyes but I actually converted a few to the consumption of deer.w/ regards

I have lived most of my life eating Biscuits, gravy, chicken fried deer meat or elk that has been boned out, pinto beans, mashed potatoes, and chili (salsa)...My mother raised us on it and I raised my kids on it, along with good beef...

Never started eating healthy until my wife went nuts about 5 years ago and decided we weren't eating right, and nothings been the same since, but she still frys up a batch now and then when I get real cranky or the grandkids come over and demand country breakfast, thats bacon and eggs, biscuits, grits, toped off with peanut butter mixed with Karo syrup on a biscuit or two, and thats breakfast, then deer meat and the above for supper. I love it when they come over and we eat like real people, she spoils them thank goodness, oh yes and for desert pour a little log cabin syrup on your deer meat, it's great... thats the cowboy way, when the nearest store is 125 miles away.

Who knows for sure? Who is going to win that lottery? Film at 11....

Been eating venison for a long while now, all I got from it is CRS. Wish I could remember what that was...

[QUOTE] Just "not thinking straight" is a "Canadian Thing" I think!

Hello JohnTheGreek, how ungracious of you. Isn't Arizona a suburb of Alberta or something? lol

Log Cabiin gee's Ray, I would have figuired you for the real McCoy Maple Syrup from Vermont and the Canadian Maritime's. Now I like to put some honey on my Venison, when its for breakfast, along with eggs hash browns bacon a quart or two of milk and a loaf of toast. Being a single guy, I get to eat what ever I want , of late I been Drinking Guiness Stout with sunday breakfast. For some reason, I was out of milk and a beer sounded pretty good. It works pretty good unless you have to go work, or operate a motor car. Get up cook breakfast, then take a nap till lunch.

Guys, this may be a stupid question, but I love deer jerky, I assume that is safe? If it isnt, I think I'll just take my chances.

Now y'all got me scared. I was going the eat deer meat tonight but.... instead I cooked up some rabbit my wife shot for me with her 44 S&W Mountain Gun [Speer shot shells ]

MMM, venison. The other pink meat!