D
Deerslayer
Guest
Good post Non-Typical......
DS
DS
jackfish
New member
I find it interesting that with the incidences of CWD in various areas, many of which are likely to have been discovered years after the first occurance of the condition, that there is no evidence that people who ate venison from these areas have a higher incidence of CJD than areas void of CWD or have there been any reported cases of vCJD attributed to CWD. I don't know what literature you have actually reviewed, but I can't find any study that actually demonstrated that TSEs are transmissible. Showing that prion folding occurs after intracerebral inoculation of PrPres or that PrPres shows up in the Peyer's patches and some of the lymphatic system after force feeding of PrPres does not demonstrate that TSEs are spread from one organism to another. What I see is they don't know where CWD came from, they don't know for sure how it spreads (maybe because it doesn't?) and they don't know for sure if it even crosses between different species. Sure looks like a lot of guessing and fear because they don't really know what the risks are, so they play it extremely safe and ride their lack of science like a white horse. Again, I have looked at many of the sources you cite. All I see is inferences and "we really don't know". Kuru is thought to be transmitted by ritualistic cannabilism? How come they don't say it is? As to my liability, I doubt anyone is going to eat the brains of a CWD afflicted deer, or a CJD afflicted person for that matter, just because of the statements I have made. I also doubt that people butchering and eating venison with no regard for the so-called precautions will contract vCJD, even in areas where CWD is evident. There just is no evidence of it happening. Fear is an interesting phenomenon. Will I follow the deer handling precautions published by the WiDNR? Yes. Will I eat the deer I shoot? Yes. If its an animal that tests positive? Well, I'll cross that road when I get there.
Nontypical
New member
jackfish,
it seems you don't understand the difficulty in proving causality in disease, and the science of epidemiology
epidemiology is a difficult science because it's always a statistical argument, not a direct demonstration of causality
here we've got a situation where the prion theory believed by most (not all, you note purdey as a skeptic) says the infectious agent is an abnormal protein
there's lots of data that supports that hypothesis
but proving it is true is quite difficult
This is true in viral diseases as well, where the infectious agents are better understood and accepted. You sidestepped the HIV example I gave above... what do you believe there? Do you believe cigarettes can cause cancer? What do you believe causes anything?
although I'm not aware of any report where vCJD has been clearly attributed to CWD...
estimates are maybe 80 million people in the UK ate BSE at some level, and about 120 cases of vCJD are reported
you do the math, it might take quite a while to see a CWD caused case of vCJD if the barrier to jumping is similar... but what if it was readily transmissible between people after jumping... aaaargghhh... read the horror scenario I suggested
the in vitro studies say the CWD prion can convert the human precursor though, so given present knowledge a risk is there, but nobody knows how big
there's a difference between letting fear run your life and being prudent, the odds of shooting yourself on the hunt or crashing the truck on the way home and dying are probably higher... but CJD isn't pretty
I firmly stand by my statement that you're being completely irresponsible posing as an authority making statements like "there is no evidence...".
in fact, there are many published papers in well respected journals (not the Med. Hypothesis that Purdey publishes in) that conflict with your assertions, you seem to be ignoring this evidence, stating it doesn't exist, to cozy up to your favorite hypothesis.
Do you really think all the biologists in these various departments of fish and game want to maximize public fear about this? Kill off the game they manage? The warnings and culls are all about being prudent.
If you're not worried about liability, maybe considering how your conscience would treat you if you do manage to influence someone to get sick will cause you to act like less of a crank.
I'm done posting on this thread trying to get you to quit acting irresponsibly. I've done my part to call you out, I wouldn't have a clear conscience letting your statements go unchallenged. Hunters can read the precautions from their game departments, the articles in the popular press (e.g. the 10/02 field and stream I just got in the mail), and the scientific literature (see the link I posted above), and make their own decisions as to your "no evidence..." statements. If they want to listen to you or Purdey or whoever, it's up to them to judge what kind of authority they're following.
You, jackfish, can decide for yourself if you'll walk away from this thread with a clear conscience.
it seems you don't understand the difficulty in proving causality in disease, and the science of epidemiology
epidemiology is a difficult science because it's always a statistical argument, not a direct demonstration of causality
here we've got a situation where the prion theory believed by most (not all, you note purdey as a skeptic) says the infectious agent is an abnormal protein
there's lots of data that supports that hypothesis
but proving it is true is quite difficult
This is true in viral diseases as well, where the infectious agents are better understood and accepted. You sidestepped the HIV example I gave above... what do you believe there? Do you believe cigarettes can cause cancer? What do you believe causes anything?
although I'm not aware of any report where vCJD has been clearly attributed to CWD...
estimates are maybe 80 million people in the UK ate BSE at some level, and about 120 cases of vCJD are reported
you do the math, it might take quite a while to see a CWD caused case of vCJD if the barrier to jumping is similar... but what if it was readily transmissible between people after jumping... aaaargghhh... read the horror scenario I suggested
the in vitro studies say the CWD prion can convert the human precursor though, so given present knowledge a risk is there, but nobody knows how big
there's a difference between letting fear run your life and being prudent, the odds of shooting yourself on the hunt or crashing the truck on the way home and dying are probably higher... but CJD isn't pretty
I firmly stand by my statement that you're being completely irresponsible posing as an authority making statements like "there is no evidence...".
in fact, there are many published papers in well respected journals (not the Med. Hypothesis that Purdey publishes in) that conflict with your assertions, you seem to be ignoring this evidence, stating it doesn't exist, to cozy up to your favorite hypothesis.
Do you really think all the biologists in these various departments of fish and game want to maximize public fear about this? Kill off the game they manage? The warnings and culls are all about being prudent.
If you're not worried about liability, maybe considering how your conscience would treat you if you do manage to influence someone to get sick will cause you to act like less of a crank.
I'm done posting on this thread trying to get you to quit acting irresponsibly. I've done my part to call you out, I wouldn't have a clear conscience letting your statements go unchallenged. Hunters can read the precautions from their game departments, the articles in the popular press (e.g. the 10/02 field and stream I just got in the mail), and the scientific literature (see the link I posted above), and make their own decisions as to your "no evidence..." statements. If they want to listen to you or Purdey or whoever, it's up to them to judge what kind of authority they're following.
You, jackfish, can decide for yourself if you'll walk away from this thread with a clear conscience.
jackfish
New member
My rejecting the mainstream TSE hypotheses is not much different than you accepting them and infering from them that CWD will make the jump to cause vCJD. I could say that your position is also irresponsible in light of the evidence. The data that some are using to make the causal link between BSE and cases of vCJD is very weak. You talk about statistical relevance, well the confidence in those studies which are now being touted by some as fact is extremely low, low enough to not show any real correlation. How do in vitro CWD prion/human precursor conversions indicate that a person will get vCJD from eating meat from an animal with CWD? The risk is NOT low, it IS unknown. Yes, there are many papers found in well-respected journals that conflict with my assertions, but not one of them proves those assertions wrong. One aspect of the literature that has been repeated is that a genesis of these types of abnormal brain conditions can be correlated to high manganese levels, low copper levels and introduced or environmental oxidants.
I never represented myself as an authority, I presented an alternative viewpoint and gave my view of what the existing literature I have reviewed tells me. If you would like me to belatedly preface those statements with "I think" or revise them to "There is no conclusive evidence..." I will gladly. But I will not retract them. You say people should worry about CWD and I don't think they should. Worry means "to afflict with mental anguish, distress or agitation." I don't think anyone should get that worked up over this. That is not my idea of being prudent. Is it prudent to follow F&G and DNR recommendations for handling deer? Sure. But you're more likely to get leptospirosis by poor handling of deer than vCJD. Again, I don't think anyone is going to die of CJD because of what I wrote here. But I guess its me that is the reactionary and should expect derision. If that makes me a crank, so be it, but I think people should explore all of the information on this phenomena and make their own decision. Right now the mainstream theories predominate. It just ain't the whole picture.
<FONT COLOR="#800080" SIZE="1">[ 09-19-2002 22:58: Message edited by: jackfish ]</font>
I never represented myself as an authority, I presented an alternative viewpoint and gave my view of what the existing literature I have reviewed tells me. If you would like me to belatedly preface those statements with "I think" or revise them to "There is no conclusive evidence..." I will gladly. But I will not retract them. You say people should worry about CWD and I don't think they should. Worry means "to afflict with mental anguish, distress or agitation." I don't think anyone should get that worked up over this. That is not my idea of being prudent. Is it prudent to follow F&G and DNR recommendations for handling deer? Sure. But you're more likely to get leptospirosis by poor handling of deer than vCJD. Again, I don't think anyone is going to die of CJD because of what I wrote here. But I guess its me that is the reactionary and should expect derision. If that makes me a crank, so be it, but I think people should explore all of the information on this phenomena and make their own decision. Right now the mainstream theories predominate. It just ain't the whole picture.
<FONT COLOR="#800080" SIZE="1">[ 09-19-2002 22:58: Message edited by: jackfish ]</font>
jackfish
New member
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 other ruminants. 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
<FONT COLOR="#800080" SIZE="1">[ 10-01-2002 15:26: Message edited by: jackfish ]</font>
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 other ruminants. 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
<FONT COLOR="#800080" SIZE="1">[ 10-01-2002 15:26: Message edited by: jackfish ]</font>
jackfish
New member
Ross Reinhold sent this to me this morning:
October 8, 2002
Re: Chronic Wasting Disease & the Wisconsin Deer Eradication Experiment
As a landowner and year-round resident within the CWD Hot Zone, I have a natural interest in digging deep beneath the rhetoric on CWD to discover the essential facts about this disease. If a fatal and communicable disease is loose in my neighborhood, I certainly want to know everything I can about it.
Many times during the last 6 months have we heard from the DNR that the Mt. Horeb area “Hot Zone” Deer Eradication Program is based on the “best science available” and built on a foundation developed by the recognized “experts in CWD.”
Unfortunately the published scientific papers have never been referenced nor have the identity of the “experts” been listed. So my neighbors, including bona-fide Ph.D. scientists, with a similar scientific curiosity and I have had to do the library research ourselves.
What we have found is disturbing. What “Science” knows for sure about CWD is very little. You could write it in large letters on a 3x5-index card. This is due in part to the fact that here-to-fore this has been an obscure, yet fatal disease, affecting a small percentage of the deer population in two sparsely populated states AND that until now the only means of testing for the presence of the disease required killing the infected animal. These two factors have significantly hindered scientific interest and study of the disease.
Secondly, the people who have been generally suggested as the “experts” are game managers and game researchers in Colorado and Wyoming. While these persons have many years of experience with the disease, and some even have the Piled High and Deep credentials attached to their name, their success in combating this deadly disease is dismal. These two states have had no success in containing CWD; they have clearly failed to find the solution.
Experts are people who hit the bull’s eye of the target, time and time again. They are not the people who miss the target entirely – as have the game managers and their consultant academics in Colorado and Wyoming.
Recent Experience with CWD
During the last 8 months, since CWD gained more widespread attention, several new cases have been discovered in locations far removed from the endemic areas of northern Colorado and southern Wyoming. Cases have been discovered among wild populations on the Western slopes of the Rockies, on the White Sands Missile Base in far southern New Mexico far from any game farm, in Minnesota, and two clusters in Wisconsin. No smoking gun, no trail of disease, not a shred of evidence linking them to the endemic areas in Colorado and Wyoming. Yet officials persist in labeling this disease highly infectious.
British researcher Mark Purdey (website: MarkPurdey.com) has been independently studying and conducting research on spongiform diseases for over a decade. His data collection and research suggests why Colorado and Wyoming officials have been so unsuccessful. Spongiform diseases are NOT highly infectious diseases and not primarily caused by direct animal to animal contact. Their roots are in genetic susceptibility and in unique environmental factors. Spongiform disease is much more akin to cancer than it is to a viral disease like West Nile Flu.
Yet in the face of their failure, CWD game managers and their academic court are slow to re-examine their foundation assumptions and take a serious look at the compelling evidence offered by renegades like Purdey. Perhaps it is as the Ojibwe express it: “White Men are Slow Learners” (Ely Echo editorial, July 7, 2002). Whatever the cause, the tunnel vision of the Wisconsin DNR has had and will continue to have drastic consequences.
If Purdey is right about genetics and environment being the primary cause, there are important implications to Wisconsin’s Grand Deer Eradication Experiment.
1) We can avoid the squandering of additional millions of dollars of taxpayer money chasing an enemy who isn’t there.
2) We can feel much more comfortable that eating venison or dressing out a deer infected with CWD will not result in human disease.
3) We need not fear that a deer 100 miles from Mt. Horeb will ‘catch’ the disease from a CWD infected deer in the Mt. Horeb area.
4) And most importantly it means that we should be doing exactly the opposite of what the DNR is doing in the designated Intensive Harvest Zone.
A Wiser and Safer Course of Action
Instead of killing and Chronically Wasting 25,000 to 50,000 deer inhabiting the Hot Zone, we should quarantine the area, stop all hunting, and establish an Intensive Research Zone.
A live deer test for CWD is currently being perfected. This will allow, for the first time ever, science to study the deer and the disease in the wild and in controlled experimental situations. We have in the Mt. Horeb area a historical opportunity to study CWD in a wild population and truly learn something significant about the causes of this disease and its methods of transmission.
Yet at great taxpayer expense, the DNR is blowing this landmark opportunity by killing off all the research subjects!!
So I ask you to join with the hundreds of concerned landowners in the Hot Zone to the bar the DNR and its army of recruits from killing deer on our lands. In doing so, we not only save the future of deer and deer hunting in our part of the state, we save millions of tax dollars, and finally protect a unique population of animals that science needs to study - alive.
If you hunt deer anywhere in Wisconsin, don’t kill what you won’t eat. And if you traditionally hunt in the Hot Zone, go north to hunt this year. There are many regions of huge DNR-caused deer overpopulation that are ripe for the spread of disease. Harvest these animals instead of Chronically Wasting the deer in our part of the state.
Ross Reinhold
Town of Vermont citizen
Editor of www.CAIDS-WI.org
October 8, 2002
Re: Chronic Wasting Disease & the Wisconsin Deer Eradication Experiment
As a landowner and year-round resident within the CWD Hot Zone, I have a natural interest in digging deep beneath the rhetoric on CWD to discover the essential facts about this disease. If a fatal and communicable disease is loose in my neighborhood, I certainly want to know everything I can about it.
Many times during the last 6 months have we heard from the DNR that the Mt. Horeb area “Hot Zone” Deer Eradication Program is based on the “best science available” and built on a foundation developed by the recognized “experts in CWD.”
Unfortunately the published scientific papers have never been referenced nor have the identity of the “experts” been listed. So my neighbors, including bona-fide Ph.D. scientists, with a similar scientific curiosity and I have had to do the library research ourselves.
What we have found is disturbing. What “Science” knows for sure about CWD is very little. You could write it in large letters on a 3x5-index card. This is due in part to the fact that here-to-fore this has been an obscure, yet fatal disease, affecting a small percentage of the deer population in two sparsely populated states AND that until now the only means of testing for the presence of the disease required killing the infected animal. These two factors have significantly hindered scientific interest and study of the disease.
Secondly, the people who have been generally suggested as the “experts” are game managers and game researchers in Colorado and Wyoming. While these persons have many years of experience with the disease, and some even have the Piled High and Deep credentials attached to their name, their success in combating this deadly disease is dismal. These two states have had no success in containing CWD; they have clearly failed to find the solution.
Experts are people who hit the bull’s eye of the target, time and time again. They are not the people who miss the target entirely – as have the game managers and their consultant academics in Colorado and Wyoming.
Recent Experience with CWD
During the last 8 months, since CWD gained more widespread attention, several new cases have been discovered in locations far removed from the endemic areas of northern Colorado and southern Wyoming. Cases have been discovered among wild populations on the Western slopes of the Rockies, on the White Sands Missile Base in far southern New Mexico far from any game farm, in Minnesota, and two clusters in Wisconsin. No smoking gun, no trail of disease, not a shred of evidence linking them to the endemic areas in Colorado and Wyoming. Yet officials persist in labeling this disease highly infectious.
British researcher Mark Purdey (website: MarkPurdey.com) has been independently studying and conducting research on spongiform diseases for over a decade. His data collection and research suggests why Colorado and Wyoming officials have been so unsuccessful. Spongiform diseases are NOT highly infectious diseases and not primarily caused by direct animal to animal contact. Their roots are in genetic susceptibility and in unique environmental factors. Spongiform disease is much more akin to cancer than it is to a viral disease like West Nile Flu.
Yet in the face of their failure, CWD game managers and their academic court are slow to re-examine their foundation assumptions and take a serious look at the compelling evidence offered by renegades like Purdey. Perhaps it is as the Ojibwe express it: “White Men are Slow Learners” (Ely Echo editorial, July 7, 2002). Whatever the cause, the tunnel vision of the Wisconsin DNR has had and will continue to have drastic consequences.
If Purdey is right about genetics and environment being the primary cause, there are important implications to Wisconsin’s Grand Deer Eradication Experiment.
1) We can avoid the squandering of additional millions of dollars of taxpayer money chasing an enemy who isn’t there.
2) We can feel much more comfortable that eating venison or dressing out a deer infected with CWD will not result in human disease.
3) We need not fear that a deer 100 miles from Mt. Horeb will ‘catch’ the disease from a CWD infected deer in the Mt. Horeb area.
4) And most importantly it means that we should be doing exactly the opposite of what the DNR is doing in the designated Intensive Harvest Zone.
A Wiser and Safer Course of Action
Instead of killing and Chronically Wasting 25,000 to 50,000 deer inhabiting the Hot Zone, we should quarantine the area, stop all hunting, and establish an Intensive Research Zone.
A live deer test for CWD is currently being perfected. This will allow, for the first time ever, science to study the deer and the disease in the wild and in controlled experimental situations. We have in the Mt. Horeb area a historical opportunity to study CWD in a wild population and truly learn something significant about the causes of this disease and its methods of transmission.
Yet at great taxpayer expense, the DNR is blowing this landmark opportunity by killing off all the research subjects!!
So I ask you to join with the hundreds of concerned landowners in the Hot Zone to the bar the DNR and its army of recruits from killing deer on our lands. In doing so, we not only save the future of deer and deer hunting in our part of the state, we save millions of tax dollars, and finally protect a unique population of animals that science needs to study - alive.
If you hunt deer anywhere in Wisconsin, don’t kill what you won’t eat. And if you traditionally hunt in the Hot Zone, go north to hunt this year. There are many regions of huge DNR-caused deer overpopulation that are ripe for the spread of disease. Harvest these animals instead of Chronically Wasting the deer in our part of the state.
Ross Reinhold
Town of Vermont citizen
Editor of www.CAIDS-WI.org
I am not sure what to think but there is a few thingd to consider here.
1. do we really know more that the bioligists at the fish and game about the cwd?
2. Are we being told the whole story from the authorities about this? why all the precautions about handling the animal if we cannot get it from it? they are not sure, thats he only thing thats for sure!
3. Wisconsin has a deer population density 10X higher than any state that ever had CWD before. this could spread so fast because of that density that the entire midwest could be infected in a couple years. I agree they need to thin the heard a lot to slow the spread until they learn more about it. the deer in wisconsin can rebound in a couple years of no-doe seasons after they find out what to do. But lets be real here, we need to admit there is a problem and bite the bullet until more is learned about it. If we ignore it and find out its deadly, it would have been a lot easier to destroy the heard in that small area before it spreads.
<FONT COLOR="#800080" SIZE="1">[ 10-10-2002 10:03: Message edited by: schmalts ]</font>
1. do we really know more that the bioligists at the fish and game about the cwd?
2. Are we being told the whole story from the authorities about this? why all the precautions about handling the animal if we cannot get it from it? they are not sure, thats he only thing thats for sure!
3. Wisconsin has a deer population density 10X higher than any state that ever had CWD before. this could spread so fast because of that density that the entire midwest could be infected in a couple years. I agree they need to thin the heard a lot to slow the spread until they learn more about it. the deer in wisconsin can rebound in a couple years of no-doe seasons after they find out what to do. But lets be real here, we need to admit there is a problem and bite the bullet until more is learned about it. If we ignore it and find out its deadly, it would have been a lot easier to destroy the heard in that small area before it spreads.
<FONT COLOR="#800080" SIZE="1">[ 10-10-2002 10:03: Message edited by: schmalts ]</font>
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