As part of my quest to identify the real causes of BSE I recently travelled to Groote Eylandt, a remote island located off the north-east Australian coast, to study a cluster of mysterious and fatal neuro-degenerative diseases – collectively known as Groote Syndrome – that had erupted among the Aboriginal people of the village of Angurugu. Unmotivated murders occur on a near weekly basis in the village.
Despite being officially blamed on the supposedly aggressive tendencies of Aboriginal people when drunk, such extreme ‘psychotic’ behaviour is unprecedented anywhere else in the Australian Aboriginal community. According to the Aboriginal elders of Angurugu, the problem developed in the late 1960s when a mining corporation started open-cast extraction of manganese nearby – causing a fine black dust of manganese dioxide to cloak the village.
As many as one in 30 people now living in Angurugu suffer from the neurological stages of Groote Syndrome. The symptoms are a grotesque mix of motor neurone failure, wasting and dementia, which reduce its victims to a state akin to ‘a stick insect trying to cross ice’.
A fierce controversy rages over the origins of Groote Syndrome. The prevailing theory blames the emergence on an inherited mutation introduced into the Aboriginal community 300 years ago. It claims that Portuguese-Macassan sailors had interbred with Aboriginal women while visiting the island for the trepang harvest. But when I spoke to the Aboriginal elders, they adamantly denied any such inter-relationships.
Furthermore, if true, why has this inherited mutation taken so many years to appear? And how, if the syndrome is an Aboriginal mutation, have white mine workers started to develop the condition as well? Given the major holes in this theory, I wasn’t surprised to discover that all the research into the disease so far has been performed by a team of academics whose work has been funded exclusively by the mining corporation. For my part, I think that the well-recognised mutagenic and neurotoxic effects of high manganese exposure could be the cause of these diseases.
If this is the case, it would be possible to treat some of the early-stage victims of Groote Syndrome with a manganese-chelating compound in the hope that the disease’s symptoms may be reversed. But until now, victims have not even been told of the existence of a possible cure. This is hardly surprising, since clinical success with such chelating treatment would betray the disease’s true cause, and thus bankrupt the mining company.
Instead current health policy is to send the victims home to die a slow, inevitable death. The BSE connection A terrible story, but what has it got to do with BSE in cattle herds thousands of miles away in the UK, or – for that matter – me? I am a working dairy farmer with first-hand experience of BSE erupting in cattle that had been purchased into my organic farm. I was struck by the fact that no cases of BSE had ever emerged in cows that had been home-reared on fully converted organic farms – despite those cattle having been permitted access to feed containing the meat and bone meal (MBM) ingredient as part of their 20 per cent conventional feed allowance decreed in the organic standards. So I embarked upon a global trek to analyse the unique environments where traditional Transmissible Spongiform Encephalopathy (TSE) had erupted in high-incidence clusters for many years.
After tramping known cluster zones in Colorado, Iceland, Slovakia, Calabria, Sardinia, Japan, et al, the results of my analysis displayed abnormally high levels of manganese and rock-bottom levels of copper, selenium and zinc in all of the food chains concerned. In adjoining disease-free areas, levels of manganese were normal. In each cluster zone tested a specific environmental source of manganese could be pinpointed. The sources could be volcanic, acid rain, steel, glass, ceramic, dye, munitions factories, lead-free petrol refineries, the take-off airspace beyond airports, fungicide and fertiliser sprays, and so forth. In addition, the customary feeding of manganese supplements (to encourage bone and antler growth, for example) could further explain the outbreaks of TSE in cattle, humans, zoo animals, deer, mink and cats.
Scientific literature also indicates a raft of neuro-degenerative disorders associated with manganese exposure over the years. The famous South Pacific clusters of Alzheimer’s, motor neurone disease and Parkinson’s – the Guam Syndrome – have all erupted in areas where manganese is at excessive levels in the local environment. From then on I became deeply sceptical of the conventional consensus on the origins of BSE and its human equivalent – variant CJD. 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 causes vCJD. (See box ‘Flaws in the official theory’.)
Fighting the government For 18 years now, I have found my work and personal integrity subjected to a steady flow of ridicule and dirty tricks. During the 1980s my farm and family became the victims of a raft of once-in-a-lifetime-type physical disasters: arson, firearms intimidation, vandalisation of my research library and communications, and infiltration by a bizarre array of bogus greens, pseudo-journalists and plain weirdos who subtly set about discrediting my social and scientific esteem. It was only when my work gained support from the likes of former minister of defence Tom King and the Prince of Wales that the physical aspects of this harassment abruptly ceased. A recent demand from the UK government departments for my personal data revealed much of what had been going on behind the scenes.
Requests by environment minister Michael Meacher to personally meet with me had been deliberately stymied by his own officials. Other documents revealed how the British Agrochemical Association had been organising a ‘joint initiative’ with the Ministry of Agriculture’s own grant-funding department to channel public funds into a live animal trial that had been deliberately designed to refute my theory. Since the BSE inquiry had rejected the official scrapie-BSE hypothesis and found in favour of some aspects of my own theory, the UK government responded by setting up a further mini-inquiry to re-examine the origins of BSE.
The resulting publication, known as the ‘Gabriel Horn Report’, employed a mix of misrepresentation and outright bogus disinformation in order to discredit the validity of my theory. When I attempted to sue the government for libel, it pleaded ‘qualified privilege’ of the expert committee and then spun out the legal communications beyond the one-year post-publication mark – thereby exempting itself from my claim. So why won’t the government listen? Regardless of the scaremongering, a basic study of the history of TSE clearly demonstrates that the disease does NOT originate from animal-to-animal contact or through ingestion of feeds contaminated with TSE brain material.
Why don’t the experts consult the wisdom of the Icelandic farmers and vets who have been living and breathing with scrapie for light years. When the first symptoms of scrapie emerge in their sheep, it is customary to slaughter the animal instantly – eating the flesh (brains and all) – before the poor animal has time to waste away. If scrapie or chronic wasting disease (CWD) can be passed on to humans via consumption – as the scientific authorities would have us believe – why have no cases of vCJD erupted in these Icelandic sheep farmers? In fact, Iceland has only ever witnessed two cases of vCJD in its entire medical history, and these victims had both hailed from the scrapie-free district in the far south of the country. Despite the failure of repeated attempts to eradicate long-term TSE hot spot regions in Colorado and Iceland by wholesale livestock slaughter and fallowing regimes, governments are still adopting the slaughter strategy as a first-choice means of control. But history has shown that TSE will invariably re-erupt as soon as fresh livestock are introduced back into slaughter areas.
Such extreme measures do little more than remove the superficial evidence of the disease. They merely mislead the public with the illusion that TSE has been controlled – a good vote-catching policy for any government. For instance, the recent discovery of new clusters of TSE in US deer has led to an official over-reaction of unprecedented proportion. A wholesale slaughter policy of the deer has been enacted throughout all CWD-endemic regions across the US. While studying in Wisconsin recently, I heard the story of a deer rancher who had retained some body tissues of his TSE-affected deer, only to find himself subjected to a gunpoint raid by wildlife officials. But who is questioning the scientific reasoning for executing this final farcical solution on these poor creatures? The policy of slaughtering a few million healthy animals across the world has been received with almost complacent acceptance.
Reports pop up with ever-increasing frequency of so-called TSE precautionary control programmes – annihilation of a herd of water buffalo in Vancouver, herds of sheep culled in Vermont, thousands of scrapie-susceptible sheep herds destroyed across Europe, 400,000 cows slaughtered in Germany – all of them healthy animals. If we can understand the cause of TSE, then we will be able to prevent, control and maybe even cure the disease. Only last month vet Terry Spraker, who oversees TSE in deer in Colorado, told me that symptoms had been reversed after treating TSE-affected deer with copper. Unfortunately, the Establishment has no interest in the cause, prevention or cure of this grotesque disease.
Its current global agenda to depopulate livestock numbers is for reasons that have nothing whatsoever to do with health risks to the human race, but more to do with envisioned profits from multinational GM proteins. Corporations have invested billions of pounds in researching and developing their GM arable protein crops and the complementary package of pesticides to go with them. So why would the Establishment spend any time or money investigating my peer-reviewed work when the outcome, if it proved my theories right, would cost them millions in compensation.
Mark Purdey lives and works in Somerset, England. A passionate environmentalist, Mark has spent his life investigating disease clusters and their causes.
For more on Mark’s fascinating work visit his website at www.markpurdey.com
MANGANESE ON THE BRAIN: THE PROBLEM The copper-bonded prion protein is found along the circadian mediated pathways that network deep into the brain (eg, in the retina, pineal gland, visual cortex, brain stem, serotonergic/sympathetic nerves, etc). When copper is in short supply in the brain the prion protein’s metal bonds become vacant – rendering the protein vulnerable to bonding with certain alternative metals, such as manganese, bismuth, silver or lithium. When present, these foreign metals may not act in the overall best interests of the organism. For instance, manganese will absorb and store up energy instead of conducting it as copper does. This blocks the flow of electromagnetic energy along the circadian pathways. Such blockages will disrupt the balance of all circadian mediated metabolism throughout the body. This explains the clinical and pathological profiles of TSE.
One of the specific characteristics of ‘trivalent’ manganese is that it can absorb the energy of sound. Acute shock bursts of sound energy can actually metamorphose the atomic structure of manganese. This creates a kind of Jekyll-and-Hyde-like transformation of manganese from its normal paramagnetic form to an abnormal ferrimagnetic one – ie, from a temporary to permanently magnetised form. Once an individual’s brain is contaminated by this form of metamorphosed manganese, any subsequent exposure to external electromagnetic fields (eg, UV, radar, cell phones, etc) will permanently charge up the manganese prions. Once the explosive threshold is exceeded, self-perpetuating ‘cluster bombs’ of free-radical-mediated neuro-degeneration erupt – creating the infamous spongiform lesions of TSE. The new strain TSEs could be explained by the current trend of increased exposures to man-made pollutants involving manganese emissions, copper-chelating chemicals (ie, the warble fly and headlice insecticides), and electromagnetic radiations (UV, mobile phones, radar, infrasound, etc). These penetrate into the central nerves and give rise to the more virulent, accelerated version of TSE, where full-blown symptoms erupt in much younger mammals than normal.
PATTERN OF EMERGENCE
Rural/coastal ecosystems (where most of the BSE clusters have been found) have become increasingly exposed to a toxic combination of manganese fertilisers and fungicides, infrasound derived from turbojet aircraft, and oxidising agents such as UV, ozone or systemic crop sprays. Town environments have ironically been spared from many of these assaults. Furthermore, this geographical pattern of emergence helps to dispel the myth that vCJD arises from ingestion of TSE-affected animal products. Meat products are consumed equally by urban and rural populations alike. The increase in oxidants relative to rural areas is partly due to the shield of smog that envelopes the majority of urban airspaces. This serves to scatter and absorb the incoming UV rays, thereby preventing the deadly UV–exhaust gas interaction with its legacy of ozone formation. The most significant increase in the burden of artificial infrasound in the UK and France can be sourced to the overflights of the Concorde supersonic aircraft. Furthermore, all of the clusters of vCJD in rural villages in the UK lie beneath the charter and routine flight paths of Concorde and low-flying military jet test routes. The afterburner turbofans employed by these supersonic aeroplanes radiate such a high intensity of low-frequency infrasound that a 100km-wide carpet of infrasonic shock is left in their wake – whether flying sub- or supersonically. Racing pigeons that have flown into this shock carpet have permanently lost their sense of magnetic orientation. A New Zealand epidemiologist reported to the BSE inquiry that the most intensive clusters of BSE had always appeared on the extreme tips of the UK’s copper-deficient west coast peninsulas. The well-used west coast test route for supersonic military and Concorde aircraft ran precisely over these BSE hot spots. Likewise, the infrasonic environs of Staten Island and Long Island in the US – both under the take-off flight paths of JF Kennedy Airport, where Concorde and other aircraft land – has demonstrated the highest incidence cluster of vCJD in the US.
Over the last two decades, increased amounts of high-concentration manganese oxide additive have been introduced into the bovine, human, pet and zoo animal food chains in Europe via a multitude of applications. These include free-access mineral licks, tablets, fertiliser and fungicide sprays, paints and petrol additives. Manganese is also present in trendy food products such as soya, which naturally bio-accumulate high levels of it from the soil. Disturbingly, manganese is added to artificial milk-substitute powders for calf and human infant consumption at levels up to 1,000 times greater than those found in normal cow and human breast milk. Excess intakes of dietary manganese pose a great risk when fed to the immature mammal, since the regulatory mechanisms of the blood-brain barrier are underdeveloped at this stage. This permits an excessive uptake of manganese and other metals into the brain. The addition of manganese to artificial milk powders explains why dairy cattle, which were invariably reared on this milk powder, suffered such a high incidence of BSE in relation to beef suckler or organic cattle, which were invariably reared on natural cow’s milk.
FLAWS IN THE HYPOTHESIS
1 The meat and bone meal (MBM) feed held responsible for the massive BSE epidemic in the UK has been exported (by the cargo boat-load) for cattle herds worldwide since the 1960s. Yet the majority of importing countries have not suffered a single case of BSE in their cattle herds to date.
2 The same is true for the cheap beef by-products blamed for causing variant CJD and which have also been exported worldwide. Only the UK and France have witnessed vCJD.
3 40,000 cases of BSE have erupted in UK cows born after the 1988 ban on MBM. In some BSE-endemic countries, more than half of their total BSE cases were born after their respective MBM bans.
4 TSE-susceptible goats and sheep were fed the same MBM ingredient, yet no cases of BSE emerged in these animals. Furthermore, animals which were never fed MBM in their feed – such as the Kudu antelope in London zoos – went down with BSE.
5 A government experimental farm at Liscombe on Exmoor was designed to produce beef on a pure grass and silage feed system. There were no MBM inclusions. Some of the cattle raised on this farm still developed BSE.
6 Not surprisingly, the UK government appeared reluctant to test its own theory. However, when several US trials attempted to reproduce BSE in cattle by feeding them with massive doses of scrapie brain material, the cattle did not develop BSE.
This article first appeared in the Ecologist November 2002