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Exploding head syndrome

Exploding head syndrome is a rare condition first reported by a British physician in 1988 (PMID 2899248) that causes the sufferer to occasionally experience a tremendously loud noise as if from within their own head, usually described as an explosion or a roar. This usually occurs within an hour or two of falling asleep, but is not the result of a dream. Although perceived as tremendously loud, the noise is usually not accompanied by pain. Attacks appear to increase and decrease in frequency over time, with several attacks occurring in a space of days or weeks followed by months of remission. Sufferers often feel a sense of terror and anxiety after an attack, accompanied by elevated heart rate. more...

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Attacks are also often accompanied by perceived flashes of light or difficulty in breathing.


The cause of exploding head syndrome is not known, though some physicians have reported a correlation with stress or extreme fatigue. The condition may develop at any time during life and women are slightly more likely to suffer from it than men. Attacks can be one-time events, or can recur.

The mechanism is also not known, though possibilities have been suggested; one is that it may be the result of a sudden movement of a middle ear component or of the eustachian tube, another is that it may be the result of a form of minor seizure in the temporal lobe where the nerve cells for hearing are located. Electroencephalograms recorded during actual attacks show unusual activity only in some sufferers, and have ruled out epileptic seizures as a cause (PMID 1896728).

Those who claim to be subject to Kundalini events occasionally report similar auditory phenomena.

Whatever the mechanism, however, it appears that exploding head syndrome is a real phenomenon and not caused by psychological disturbances. It is not thought to be medically dangerous, although it is often distressing to experience. Note that EHS does not, in fact, cause the head to explode.


Symptoms may be resolve spontaneously over time. It may be helpful to reassure the patient that this symptom is harmless. Clomipramine has been used in 3 patients, who experienced immediate relief from this condition (PMID 1896728).


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The environmental origins of TSEs: the ferrimagneto-prion theory
From Townsend Letter for Doctors and Patients, 7/1/04 by Mark Purdey

The White Sands Missile Range is an extensive spread of US military controlled cacti country that spans the southernmost extremes of the San Andres mountain ridge. There is an eerie atmosphere to the place.

A Department of Natural Resources truck kicks up the dust across the dried out canyon, its engines reverberating in the quiet air. It stops at the main entrance gates along the perimeter fence. One of the wildlife officers gets out and walks to security, seemingly oblivious to the distant thump of a missile exploding across the range. He is clearly preoccupied with the more important task of slaughtering animals who have succumbed to a so-called "hyperinfectious" disease. The truck is soon on its way, disappearing within the thousands of acres of parched military compound.

They've come to investigate yet another new eruption of chronic wasting disease (CWD) in the USA--the deer equivalent of 'mad cow disease.' This outbreak is particularly significant, in that it represents the first cases of a transmissible spongiform encephalopathy (TSE) disease recorded in a deer herd within the state of New Mexico. Furthermore, the affected herd has been confined within the perimeters of this missile range for several decades.

This latest epidemiological aberration delivers a serious challenge to the viability of the conventional consensus on the origins of CWD. It has shaken the cornerstones of institutionalized 'expertise,' bringing into question those veterinarians who have opted for the assumption that some unknown "hyperinfectious" agent is spreading via body to body contact through the deer populations.

So how did the 'infectious agent' jump the 500 mile gap between the long standing CWD hotspot zone in Colorado and the CWD-free deer residing within the White Sands Missile Range? The 'experts' were baffled. But, true to form, this latest challenge to the official theory was conveniently obfuscated into oblivion; outcast as some illusory mirage that just happened one day in the New Mexico desert.

But the answer is only evident to those who care to scratch a bit deeper than the dust. For they cannot help but notice some overt environmental features that exclusively predominate this unique location. A package of factors which are invariably shared by every single TSE cluster location around the world.

Before the military came, White Sands was an industrial center for the mining of the manganese oxide and wulfenite ores (NB; wulfenite contains the copper chelating molybdenum metal). And since the military have occupied the range, the US authorities have been actively engaged in monitoring the unique intensity of infrasonic shock bursts that are radiated by the explosions of their missiles. The poor deer herd has played guinea pig to an unwitting experiment that has cracked the causal riddle of spongiform disease.

The BSE debacle

Since 1986, the infamous novel neurodegenerative syndrome, BSE and vCJD, has insidiously blighted the heartbeat of British rural life. The disease has annihilated thousands of cattle and a growing number of young people, as well as creating a fierce battleground between nations, vested interests, political parties, farmers, victim support groups and consumers. More recently, the shock waves of the BSE debacle have ricocheted around the entire world, reaching as far afield as Japan and North America.

Yet despite the severity of the mad cow legacy, little genuine attempt has been made to crack the causal riddle of these diseases; thereby leaving us devoid of insight into measures that would best cure, control and, better still, prevent this disease.

But hard scientific evidence is being amassed which indicates that vCJD and BSE could both result from separate exposure of bovines and humans to the same package of toxic environmental factors--ferrimagnetic metals and low frequency sonic shock--and not from the ingestion of the one species by the other. If such a polemic hypothesis continues to accumulate momentum, a radical upheaval of the status quo mindset can be expected.

As a working livestock farmer and TSE researcher with first hand experience of BSE erupting in cattle that had been purchased and brought into my organic farm, I was struck by the fact that no cases of BSE had ever emerged in cows that had been born and raised on fully converted organic farms, despite those cattle having been permitted access to the feed that contained the incriminated meat and bone meal (MBM) ingredient--as part of their 20% conventional feedingstuff allowance decreed in the organic standards at that time.

In this respect, I developed a hunch that the resistance of organic livestock farmers to comply with a UK compulsory livestock chemical treatment program using systemic organo dithiophosphorus (OP) insecticides--toxic chemicals derived from the OP military nerve agents--might offer an explanation for the total absence of BSE in 'home raised' organic cattle across the UK.

In 1982 measures were passed that enforced twice annual application of a uniquely concentrated dose (20 mg/kg bodyweight) of a systemic acting organodithiophosphate insecticide for the control of warbles on UK cattle. Amongst a myriad of toxicological effects, the systemic types of dithiophosphate can chelate copper and open up the blood brain barrier; thereby disturbing the overall crucial balance of metals in the brain. I was therefore not surprised to witness BSE rearing its ugly head in the UK cattle herd in 1986; which, in my opinion, was partly a direct legacy of the UK government's compulsory 'high dose' warble fly campaign. The few other European countries who instigated warble fly campaigns (eg; France, Switzerland, Ireland, etc.) used lower doses of insecticide, and, not surprisingly, developed proportionately fewer cases of BSE as a result.

From then on, I became deeply skeptical of the conventional consensus on the origins of BSE and its human equivalent, vCJD. There were just too many radical flaws blighting the hypothesis that bovine ingestion of micro doses of scrapie contaminated MBM lead to BSE. Equally flawed was the follow up theory that human ingestion of BSE-contaminated beef caused vCJD.

The hyperinfectious hypothesis was based upon a single strand of evidence--that TSEs could be transmitted via injections of TSE-diseased brain tissues into unfortunate laboratory animals. Yet, various other diseases, such as familial Alzheimer's disease, thyroiditis and toxic metal encephalopathies have been transmitted in this way. So why aren't the health authorities panicking about the supposed 'hyperinfectious' capacities of these other diseases?

The Flaws in the Conventional Hypothesis

1. Thousands of tons of the BSE-incriminated meat and bone meal (MBM) feed were exported as cattle feed during the 1970s/1980s/1990s to countries that have remained BSE-free to date--eg, South Africa, Sweden, Eastern Europe, Middle East, India, Third World, etc.

2. Relaxation in the temperature/manufacturing techniques of the MBM rendering process in the UK was blamed for permitting the survival of the scrapie agent in the sheep brain material; thereby enabling the "agent" to jump across into cattle, producing BSE. But none of these alterations were exclusive to the UK plants. For instance, other scrapie endemic countries such as USA and Scandinavia had adopted the same continuous flow system of rendering five years before the UK, yet these countries have remained BSE-free. Furthermore, the pathogenic, 'infectious' capacity of the scrapie agent remains active after heating to temperatures up to 700 degrees--way above the 150 degree temperatures employed in the supposedly 'safe' rendering processes operating in pre BSE days.

3. Several live animal trials in the USA failed to induce BSE in cattle after feeding/injecting them with massive doses of scrapie-contaminated brain tissue. Furthermore, no cases of BSE have developed in 1000 cows that were experimentally challenged with high doses of MBM feed/innoculant on a Department of Agriculture farm at High Mowbray in Yorkshire, UK.

4. Forty thousand plus cows that were born after the UK's 1988 ban on MBM incorporation into cattle feed have still developed BSE.

5. Several countries such as Ireland, Portugal and France have witnessed a greater number of BSE cases in cows born after their respective bans on MBM than in cows born before their bans.

6. There have been no cases of BSE in other TSE-susceptible ruminants in the UK, such as goats and sheep, despite the customary inclusion of the same MBM protein source in their feeds.

7. Four of the original five kudu antelope that developed BSE at the London zoo had not had any possible access to MBM-containing feeds.

8. The UK government's former experimental farm at Liscombe on Exmoor was designed to raise suckler beef cattle on a pure grass/silage system--without resort to feeding any MBM containing concentrated feeds at all. Yet BSE struck down four animals on this holding.

9. It is customary for Icelandic sheep farmers to slaughter and eat their scrapie-affected sheep (brains included) immediately the first symptoms of this rapid wasting disease are recognised. Yet, no cases of CJD have been recorded in Icelandic sheep farmers.

10. The infamous mechanically retrieved meat products/baby foods blamed for causing vCJD in the UK were exported all over the world to countries where vCJD has not erupted to date.

11. BSE fails to fulfill 'Koch's postulates'--the yardstick for gauging whether a given disease stems from infectious origins.

Hyperinfectious Hysteria takes hold

Despite the myriad of epidemiological flaws and millions of pounds worth of research failing to ascertain any association between the origin of these diseases and the scrapie agent, the whole propaganda myth that BSE was caused by scrapie became impregnated as 'gospel' into mainstream public/professional mentality.

It is easy to see how the momentum of such a reductionist mindset took hold; the media loved the theory because they could drum up a viral holocaust-horror scoop. The farming industry could get their beef sales back on the road by deluding consumers that the causal agent had been eliminated. The vegetarian lobby found themselves with a powerful propaganda weapon on their plate, whilst the scientific institutions could carry on, drawing generous funding for their hyperinfectious witch hunt without the embarrassment of having to account for years of barking up the wrong tree. And the government could conveniently offload the blame onto the vagaries of some naturally occurring 'nasty' for which no vested interest or official directive could ever be held accountable.

Governments of the BSE-affected countries rapidly found themselves cornered into providing 'quick fix' remedies to appease the mounting intensity of political and economic pressures levied on them by their BSE-free neighbours.

Sound scientific reasoning has been forced to give way to the panic response; where wholesale slaughter regimes are enacted across the TSE affected regions, despite well documented historical evidence that these measures have repeatedly failed to eradicate TSEs in the longstanding scrapie and CWD hotspot regions across Iceland and Colorado--at great expense to the taxpayer, the farmer and animal life.

Cluster Buster

As a TSE field scientist, my observations and research findings led me to question the scientific validity of the conventional consensus on the origins of TSE. I felt convinced that some key package of environmental factors, such as the copper chelating OP warble fly insecticides, played a primary role in the cause of TSEs, and so I embarked on a global investigation in search of the etiological needles in the causal haystack.

I carried out total environmental analyses of the soil, water and foodchains in various ecosystems of Japan, Slovakia, Italy, Sardinia, Sicily, Iceland, Colorado, Wisconsin, etc, where longterm clusters of TSE have emerged in mammalian populations who are largely self-sufficient upon the local foodchain. I also sampled the adjoining TSE-free areas as controls.

My results indicated that high levels of specific metals such as manganese, uranium and strontium, in combination with deficiencies of copper, constituted an abnormal mineral imbalance that was common to every TSE cluster region that I had analysed. The levels returned to normal in TSE-free adjoining areas.

I also identified the co-presence of high intensities of low frequency sonic shockbursts in all of these TSE cluster environments, which stemmed from a variety of prominent sources; such as low flying military or concorde jets, quarry and military explosions, volcanic/earthquake tectonic rift lines, thunder and electric storms, etc.

I compiled and published a hypothesis which proposed that this abnormal mineral imbalance compromised the ability of the brain to protect itself against the neurotoxic effects of incoming sonic shocks from the external environment.

Copper prion proteins as the 'conductors' and Manganese prion proteins as the 'blockers' of electromagnetic energy flow

Whilst endorsing the well-established view that a malformed version of a native brain protein, known as the prion protein, plays a pivotal role in the pathogenesis of TSEs, I did not subscribe to the extreme view that this proteinaceous particle acted as the hyperinfectious TSE agent.

Given the mystery surrounding the healthy function of this elusive protein, I became interested in the fact that the normal prion protein had been shown to bond onto copper in the healthy brain, as well as performing a functional role in the mediation of the circadian rhythm. I proposed that the copper component of the normal healthy prion protein plays a role in the conduction of electromagnetic energy along the circadian/auditory pathways of magnetic superexchange; where a linear chain of paramagnetic copper atoms (bonded to prion proteins) provides a 'metal to metal to metal' motorway which distributes the electromagnetic energy of light and sound (received at the retina and cochlear) around the tissues for energizing the circadian mediated cycles of sleep, sex, behaviour, heartbeat, cell growth/repair and immune response--locations where the prion protein is intensively expressed.

So once the crucial supply of copper is curtailed in the brain--due to straightforward environmental copper deficiency or exposure to copper chelating OP insecticides, etc.--the prion protein's metal bonds become vacant, rendering the protein vulnerable to bonding with certain alternative replacement metals, such as manganese, uranium or strontium, which have binding affinity for the metal domains on prion protein. But once attached, these foreign substitutes may not act in the overall best interests of the organism, particularly if the invasive metal is in 'ferrimagnetic' and/or in 'radioactive' form.

For instance, once a ferrimagnetic manganese 3+ or strontium 90 atom substitutes at the vacant copper bonds on prion protein, the field-inducing influence of the ferrimagnetically-ordered atoms will progressively corrupt the circadian mediated pathways of electromagnetic superexchange throughout the brain; whereby a status of permanent magnetic charge is spread much like a domino-style, contagious corruption which jumps from metal bond to metal bond, from prion to prion. This phenomena is well illustrated by the classic college physics experiment, where a magnet is placed alongside a steel nail and the force field of the magnet rapidly magnetises the adjoining nail.

So once an individual's brain is contaminated by this freaky form of ferrimagnetic manganese or strontium, any subsequent exposure to external electromagnetic fields (eg, UV, sound waves, radar, cell phones, etc.) will permanently charge up the ferrimagnetically-ordered manganese prions to saturation point.

In this respect the TSE diseased brain can be likened to a solar powered battery on continuous charge; where the manganese loaded/copper depleted brain is no longer equipped to deal with the incoming surges of electromagnetic energy from the external environment. Instead of utilising this energy for the body's own vital requirements, its conduction is blocked and perverted into a potent force field for neuronal suicide; whereby the magnetically saturated atoms emit intensive magnetic fields, which, in turn, generate self-perpetuating 'cluster bombs' of free radical-mediated spongiform neurodegeneration. TSE ensues.

Does the rogue ferrimagnetic metal, co-partner of the misfolded prion protein, serve as the infectious/transmissible component in TSEs?

This theory explains why the so-called 'hyperinfectious' property of the prion is a misnomer. It is the toxic ferrimagnetic metal component of the prion that serves as the so-called 'infectious' pathogenic agent in TSEs. So whenever scientists inoculate unfortunate lab animals with TSE brain tissues (eg tissues contaminated with this rogue type of manganese or strontium atom) and effectively transmit TSE, they are actually transmitting a 'magnetic field inducing capacity' that is carried along with the ferrimagnetically ordered metal contaminant into the recipient animals, who, in turn, develop TSE.

Furthermore, the concept of the rogue ferrimagnetic manganese atom as the 'TSE agent' also explains why the so called 'infectious' pathogenic capacity of the prion can survive heating to temperatures in excess of 500 degrees--since ferrimagnetic metals will hold onto their magnetic charge until they are heated to temperatures beyond their respective 'curie point' temperature. (eg, 550 degrees for manganese 3+)--whence its magnetic energy is instantly drained.

Laboratory support for the TSE environmental origin theory

Several laboratory studies have come out in strong support of the mainstay of these environmental observations, suggesting that the abnormal mineral template common to TSE ecosystems represents more than an incidental finding. For instance, Cambridge University demonstrated that the prion protein adopts its TSE deformed shape after manganese has been added to copper depleted prion protein cell cultures, whilst the US Prion Surveillance Centre at Case Western University in Cleveland observed a ten fold increase in manganese levels and 50% reduction of copper in sCJD diseased brain tissues.

From the soil to the brain; the environmental dynamics of TSE pathogenesis

Interestingly, neuropathologists working on post-mortem TSE diagnosis in Sardinia, Iceland and Colorado, report worn down, soil-stained incisor teeth as well as a deposition of grit/soil in the gastro tracts of the carcasses of scrapie and CWD casualties that are sent in for analyses. These unusual phenomena could be explained by the fact that both CWD and scrapie have a tendency to erupt in overpopulated ruminant populations who are overgrazing short-cropped pastures in drought stricken areas; indicating that these hard pressed, grazing animals would be taking in significantly larger amounts of top soil than normal.

Likewise, CJD has a tendency to erupt in self sufficient and/or rural based human populations whose work and lifestyles necessitate closer contact with the soil.

My studies have observed that TSE clusters arise in mammalian populations who are dependent upon certain geological soil types that have been subjected to various environmental 'stress' influences (eg; infrasonic vibrational shocks, fire, lightning strikes, intensive ultraviolet radiation, drainage/liming). These influences can trigger a metamagnetic transition of certain iron, manganese 3+, uranium, strontium compounds in the soil (and atmospheres) which can open up a quantum capacity for absorption of select frequencies of phonons, photons or thermal energy that are incoming from the external environment. For instance, low frequencies of acoustic-vibration shock energy can actually metamorphose the octahedral crystalline lattice of some metallic compounds, inducing a metamagnetic transmutation of the atom from paramagnetic to ferrimagnetic form.

So in areas where the rogue ferrimagnetic manganese 3+, uranium or strontium species of metal is at high levels in the soil, any intake of top soil into the guts of grazing ruminants is likely to result in the increased uptake of these rogue metals into their biosystem, and, in certain circumstances, into their brain.

Furthermore, overpopulation of cervids in the CWD areas, has also led to increased browsing of juniper/pine and of locally farmed alfalfa crops as a means of bolstering their impoverished diet. These plants concentrate strontium and manganese to excessively high levels (Author's latest unpublished observations 2002/2003), so could represent a source of the rogue metals in conjunction with the more direct source from the soil.

Alternatively, the actual sonic shock induced metamagnetic transmutation could be triggered in the metal atoms within the living brain itself. A good example of this phenomena is possibly illustrated in the context of the racing pigeons who had flown into the 100 km shockwave boom carpet left in the wake of the Concorde supersonic aircraft and had permanently lost their sense of magnetic orientation as a result. Furthermore, cell culture studies have also shown that a sound wave challenge will proliferate the mysterious multireplicating property of the prion protein.

It is proposed that the long standing, less aggressive, traditional strains of TSE are largely caused by exposure to foodchains that are contaminated by naturally occurring sources of toxic ferrimagnetic metals (manganese, thorium, strontium from volcanic emissions, etc.) and deficiencies of copper; along with exposure to intensive shockbursts of naturally occurring sources of low frequency acoustic waves which emanate from the movement of tectonic fault lines (during earthquake, volcanic activities) or from thunder/lightning storms.

Whereas, the more aggressive, accelerated version of new strain TSEs (BSE/vCJD) that has emerged more recently in younger mammals, are caused by exposure to the more intensive artificial sources of these same ecofactors. In this respect, it is proposed that the UK's BSE and vCJD 1986-2000 epidemics were caused by the simultaneous exposure to:

1. The soils/atmospheres that were contaminated with high levels of radioactive strontium 90 after the emissions from the 1986 Chernobyl atomic leak were rained down over North Western Europe (UK, and to a lesser extent Brittany, Ireland, etc.)--the precise region which was shortly to become the first ever BSE hotspot region in the world.

2. The systemic acting 'copper chelating' types of organo dithiophosphate insecticide that were intensively used for warble fly/head lice/flea/food crop treatment around this time; thereby starving the prion protein of its copper co partner, subsequently rendering the protein's vacant metal domains to binding up with any replacement metals that are at 'superfluous' levels within the brain; eg; the rogue radioactive strontium 90.

The resulting mineral imbalance impairs the ability of the mammalian brain to deal with the ever increasing challenge of sonic shocks from the external environment.

The Canadian context

The Canadian authorities should make a concerted attempt to identify the true origins of their TSE cases. My own preliminary survey has identified some of the key TSE risk phenomena in the environments where TSE has erupted in Alberta and Saskatchewan to date. The two farmed deer diagnosed with CWD were both raised on a farm that was directly under the takeoff flight path of a recently closed military jet base on the northern side of Edmonton.

The 'nidus' of the new variant TSE cases that have erupted in Canada so far, have involved two mammals (a human and cow) that had both originated from around the Sandhills district of Saskatchewan. Identical to the other TSE hotspot regions across North America, the soil is copper deficient, high in uranium/strontium and is of the drought prone, sandy type. The vegetation is also predominated by the juniper bush. Interestingly, the largest military tank test shelling range in North America, Camp Wainwright, is also located in the middle of this area, where the low frequency acoustic shockbursts from the tank shelling practice reverberate throughout the summer period.

Interestingly, all Canadian cases of CWD in wild deer have also originated from the Sandhills area to date. In fact, the first case of CWD was purportedly observed in a deer that was picked up staggering around in dazed condition on the military range itself.

Understanding the true causes of TSEs provides the best insight into measures that would best cure, control and, more importantly, prevent these grotesque diseases. Given the potential financial losses that could be incurred by the Canadian/North American economy as a result of the recent outbreaks of TSEs in deer and cattle herds, it would seem wise for the appropriate authorities to break ranks with the mainstream reductionist mindset on the origins of TSE and adopt an alternative foolproof strategy for getting to the root of this problem, rather than 'cuckooing' out the same old stereotype protocol of control measures that have invariably failed to properly control a single outbreak of TSE to date.

Wholesale slaughter measures; the final farcical solution?

The epidemiological and experimental evidence amassed to date points to the fact that TSEs are caused by a clearcut combination of genetic and toxic environmental factors. And, despite the universal scaremongering over the 'hyperinfectious' nature of the prion, an impartial study of the epidemiological history of TSEs clearly demonstrates that this disease does NOT originate from animal to animal contact or through ingestion of feeds contaminated with TSE brain material. So why do the authorities continue to treat these diseases as if they stem solely from hyperinfectious origins?

The reasons for such an irrational, Pavlovian-like stance of the Establishment towards the environmental perspectives of TSEs probably hangs upon issues that are more to do with protecting academic egos, professional reputations and the vested interests of the TSE institutions/key advisors, than with promoting sound scientific argument. But the main reason must undoubtably stem from the fear of massive compensation claims, should issues such as government mandated use of copper chelating 'OP warblecides' (re the massive BSE epidemic in the UK) or leakage of radioactive metals from power or military facilities ever prove to be partially accountable for TSE causation at the end of the day.

Despite the repeated failure of wholesale livestock slaughter /fallowing regimes to eradicate long established TSE hotspot regions in Colorado and Iceland since the 1970s, governments are still adopting this same slaughter strategy as a first choice means of control today. But history has shown that TSEs will invariably re-erupt as soon as fresh livestock are introduced back into the slaughtered out areas; supporting the idea that the environmental causes of TSE are still well and truly wedded to the local food chain.

Such extreme measures do little more than remove the superficial evidence of the disease. They merely mislead the public into the illusory notion that TSE has been controlled (a good vote catching policy for any government). But who is questioning the scientific reasoning for executing this final farcical solution on these poor creatures. For the unilateral adoption of a policy of 'totalitarian overkill' of a few million healthy animals across the world has been received with almost complacent acceptance. Such perverse and senseless 'carry ons' have sadly become the daily 'non-stories' of our modern times. Reports pop up with ever increasing frequency of so called TSE precautionary slaughter control programmes being enacted after 3% or more animals in a flock prove positive to the TSE genotype test; an innocuous, endemic phenomena that has existed in the sheep flocks across countries like Australia for light years. Countries where clinical scrapie has never emerged, presumably because the TSE environmental triggers are not present there.

Nonetheless, despite the total absence of any sound scientific requirement, the prophylactic annihilation of livestock still carries on--a herd of water buffalo in Vancouver, deer herds across North America, sheep flocks from Vermont, hundreds of cows slaughtered in Germany, plus thousands of scrapie susceptible traditional sheep and goat herds erased from the European hillsides--all healthy animals.


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