Extract: Despite the severity of the BSE 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.
Hard evidence has been amassed which indicates that vCJD and BSE could both result from separate exposure of bovines and humans to the same set of toxic environmental factors - manganese and oxidizing agents; and not from the ingestion of the one by the other. If such a polemic hypothesis continues to accumulate momentum, a radical upheaval of the status quo mindset can be expected.Despite this discovery being substantiated by both field and laboratory observations, the resulting published data has been outright dismissed by Establishment bodies. Furthermore, all funding proposals aimed at furthering this line of research have been irrationally rebuffed at peer review. Contrary to the positive recommendations of the 1999 BSE Phillips Inquiry report to the UK government for funding my work, rejection of grant proposals continue to present day, including one submission aimed at developing a feasible cure for vCJD !
'Rida' is the Icelandic for transmissible spongiform disease)
An underground scientific journey into the origins of spongiform disease.
by Mark Purdey.
Since 1986, the infamous novel neurodegenerative syndrome , BSE and vCJD , has insidiously blighted the heartbeat of English 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, victims and consumers.
But despite the severity of the BSE 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 this story shines a ray of light over the whole debacle. It charters my own eco-detective escapades and original field investigations which ran in tandem with the laboratory quest of Cambridge Uni biochemist, Dr David Brown. These combined works have gone a long way towards unearthing the truth underpinning the original cause of these grotesque diseases.
Hard evidence has been amassed which indicates that vCJD and BSE could both result from separate exposure of bovines and humans to the same set of toxic environmental factors - manganese and oxidizing agents; and not from the ingestion of the one by the other. If such a polemic hypothesis continues to accumulate momentum, a radical upheaval of the status quo mindset can be expected.
Despite this discovery being substantiated by both field and laboratory observations, the resulting published data has been outright dismissed by Establishment bodies. Furthermore, all funding proposals aimed at furthering this line of research have been irrationally rebuffed at peer review.
Contrary to the positive recommendations of the 1999 BSE Phillip’s Inquiry report to the UK government for funding my work, rejection of grant proposals continue to present day, including one submission aimed at developing a feasible cure for vCJD !
The Lone Voyager
My work first came to the fore after successfully quashing the UK government’s compulsory warble fly eradication regime in the high courts in 1984. This exempted my farming business from treating our dairy herd with a systemic organo phosphorus (OP) insecticide - a toxic chemical which, amongst a myriad of toxicological effects, disturbs the 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 a direct legacy of the UK government’s warble fly mandate that enforced exclusively high doses of systemic OP insecticides- doses which were four times higher than those applied in the few other countries who used this type of insecticide.
I was a working dairy farmer with first hand experience of BSE erupting in cattle that had been purchased into my organic farm. But I was struck by the fact that no cases of BSE had ever emerged in home reared cows on fully converted organic farms, despite those cattle having been permitted access to the feed that contained the meat and bone meal (MBM) ingredient - as part of their 20% conventional feedingstuff allowance decreed in the organic standards.
From then on, I became deeply sceptical 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 Flaws in the Conventional Hypothesis ;
1. Thousands of tons of the incriminated UK MBM feed was exported for 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. NB; MBM was exported in both straight form, as well as an ingredient of the compounded concentrated feed pellets.
2. Changes in the temperature / manufacturing techniques of the MBM
rendering process in the UK were blamed for permitting the survival of the
scrapie agent in dead sheeps’ brain; thereby enabling the “agent” to jump
across into cattle, producing BSE. Yet in other scrapie endemic countries,
such as USA and Scandinavea, the exact same continuous flow system of
rendering was adopted five years before the UK, yet these countries
3. Several US trials failed to invoke BSE in cattle after feeding/injecting them
with massive doses of scrapie contaminated brain tissue.
4. Forty thousand plus cows that were born after the UK’s 1988 ban on MBM
inclusion in cattle feed have still developed BSE. Furthermore, a small
number of cows born after the further additional 1996 ban on MBM
inclusion in feed destined for all types of livestock have already developed
5. Several countries such as Ireland, Portugal and France have witnessed
more cases of BSE 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
(Transmissible Spongiform encephalopathy ) ruminants such as goats and
sheep in the UK 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 had no 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 concentrated feeds at all. Yet BSE struck
down four animals on this holding.
9. The UK’s 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. Likewise, the practise of ‘skull splitting’ in
small rural butchers was offered as an explanation for the growing number
of vCJD clusters in rural areas. But this was practised by the smaller
butchers all over the UK.
10. It is hard to see how the so called infectious prion agent; a malformed
prion protein that is resistant to all forms of enzyme digestion can be
absorbed as an intact protein across the gut wall, thereby infecting its
host with TSE.
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.
But It is easy to see how such a reductionist mindset took ahold ; The media loved the theory because they could drum up a viral holocaust-horror scoop. The vegetarian lobby found themselves landed with a powerful propaganda weapon on their plate, whilst the scientific institutions could carry on drawing generous funding for their hyperinfectious witchhunt 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 phenomena for which no vested interest or official directive could ever be held accountable.
And more recently, the multinational corporations have been capitalising off this hyperinfectious ‘prion’ theory too; by coercing governments and their media spin docters to scare consumers away from so called ‘prion contaminated’ livestock and organically grown protein sources.
Perhaps it is no surprise that these same corporations have been simultaneously buying up vast tracts of cheap farmland across Eastern Europe, third world countries, North America to expand their GM soya protein empire. And then dollar profits gleened from the package of agrichemicals and GM seeds required to grow arable crop proteins, such as soya, greatly exceeds that gleened from the zero pesticide inputs required for growing grass to produce meat and milk.
Prion Origins; the quest for primary cause.
It is well demonstrated that the central pathological hallmark of all types of spongiform disease pivots upon the presence of a malformed native protein - known as the ‘prion’ - in the nervous system of diseased mammals. But noone yet understands how and why this ‘prion’ is originally formed in the natural world.
I became interested in the possibilty that the systemic OP warble fly insecticides - which had to be poured along backline of the cow just millimetres away from the prion protein expressing cells in the spinal cord - may trigger off this malformation in some way; thereby serving as the primary cause of the disease.
It was well recognised that OP insecticides exert their toxic effects in mammals by deforming the molecular shape of various nerve proteins; those malformed proteins consequently cease to perform their proper function in the brain. But noone had ever considered that a similar style molecular interaction may occur between OPs and the prion protein.
After many abortive attempts to coerce the Establishment into running the correct laboratory test, I eventually managed to raise funds from wellwishers and personal loans to finance Dr Stephen Whatley of the Institute of Psychiatry in London to challenge brain cell cultures with the OP phosmet - the actual OP used at uniquely high doses on UK farms.
Amazingly, these trials demonstrated that the OP altered the cellular metabolism of prion protein in some of the ways observed in the early stages of spongiform disease - suggesting that phosmet exposure may render mammals more susceptible to the disease. Unfortunately, these experiments did not produce the key deformation of the prion protein that is seen in TSEs. I returned to square one; assuming that OPs in combination with a further factor X, could fulfill the final missing link in the causal jigsaw.
The Cluster Buster
Having grown exhausted by the vortex of the mad politico-medico-multinational grand alliance that had successfully hijacked and cul de sac’ed all UK scientific research into TSEs. I embarked upon a refreshing global trek to analyse the unique environments where traditional TSEs had erupted as high incidence clusters for many years.
After tramping the most clearcut TSE cluster zones in Colorado, Iceland, Slovakia, Calabria, Sardinia, etc, where an assortment of animals and humans had developed TSE, my analytical results displayed abnormally high levels of the metal manganese, and rockbottom levels of copper, selenium and zinc in all of these food chains in common. Levels of manganese returned to normal in adjoining disease-free areas.
The Men from Manganese.
A specific environmental source of manganese could be pinpointed in each cluster zone tested, where each habitat occupied by the TSE affected species in question could be directly connected to the atmospheric fall out of some naturally occurring or industrial source of combusted manganese oxide; eg stemming from volcanic, acid rain, steel/ glass/ ceramic /dye/munitions factories, lead-free petrol refineries, the take off airspace beyond airports, etc.
My observations enabled me to compile / publish a holistic hypothesis on the aetiology of TSEs, which lead to my connecting with the pioneering laboratory studies of Dr David Brown at Cambridge; a widely published biochemical expert who had pursued his ground breaking studies to demonstrate the function of this elusive prion protein.
Dr Brown not only demonstrated that the prion protein bonds to copper in the normal healthy brain, but also revealed that this copper-protein can exert an anti oxidant function.
Brown’s lab studies were complementary to my field studies; thereby providing the other half of the neccessary ground work upon which I devised a hypothesis proposing that manganese could substitute itself at the vacant copper site on the prion protein; this aberrant substitution ocurring in susceptible mammals who were self sufficient upon high manganese / low copper foodchains.
I considered that this manganese substitution could produce the all important deformation of the prion protein that is considered so crucial to the development of TSE. So David Brown ran the neccessary cell culture experiments in which he introduced manganese into cells which manufacture prion protein, and he produced just that - the key deformation of the prion protein which the earlier tests using OPs had failed to create.
Furthermore, follow up trials by Case Western Uni (Cleveland) and a Frence team ran separate post mortem analyses of brain tissue taken from those who had died of conventional CJD - once again revealing the same pattern of high manganese/ low copper as identified in TSE foodchains; a ten fold increase of manganese levels and 50 % reduction in copper in relation to control brains drawn from those who had died of natural causes
Every storm cloud has a silver lining.
A few other TSE cluster hotspots had demonstrated the same low copper connection, but had interestingly demonstrated high levels of another potentially toxic transition metal, ‘silver’, as well as manganese. Much like manganese, silver will also readily substitute at copper ligands on prion proteins . These environments were simply silver mining areas where local soils were naturally high in silver, or areas centred around ski resorts , reservoirs, airport flight paths, coastal districts, where extensive aerial spraying of weather modifying silver iodide ‘cloud seeding’ chemicals had been used for inducing rainfall/snowfall and cloud/fog dispersion.
Further daylight on TSEs - the deadly oxidative connection unleashed.
But each time my trek lead me to a newTSE hotspot, I found myself face to face with the same type of high altitude, snow covered, pine tree, pre cambrian terrain. This always reminded me of my first glimpse of chronic wasting countryside where the TSE affected deer and elk populations roamed in Colorado - the snow peaked Rocky Mountain Front Range, sawtoothing the July skyline beyond the parched out Denver Plain. Putting aside the common high manganese / low copper connection, this common geographical association with TSE cluster regions continued to baffle me.
But after arriving at the Calabrian village where 20 cases of CJD had emerged since 1995, the relevance of this geographical connection to TSE finally gelled. The houses in this village were newly constructed out of bright white concrete sections - unusual for this area. Furthermore the houses were couched within a sun parched, glaring basin of bare white sandstone terrain, producing all the prerequisites required for a most intensive ultra violet (UV) hotspot location; This experience immediately connected me across to the well recognised ‘high UV’ nature of high altitude, snow covered terrain - the common geographical thread interlinking the Icelandic, Colorado, Slovak cluster ecosystems in my study; areas also impacted by the oxidizing effects of ozone gas which is formed by the interaction of UV with the terpine haze exuding from the pine trees common to these regions.
The UV prerequisite also explained other missing links in the science of traditional TSEs - such as the way in which initial pathological damage of TSE manifests itself within the retina, the eyelid or skin of the affected mammal - external surfaces having front line exposure to sunlight . Plus the fact that the normal , healthy form of copper bound prion protein is specifically expressed in tissues whose metabolism is regulated by the circadian daylight / darkness rythmn; hence the prion protein is found along the pathways which conduct the electromagnetic energy generated by ultraviolet light around the brain - eg , in the retina, pineal gland ,glial cells, visual cortex, hypothalamus, pituitary, brain stem, immune response system, tumour cells and in nerve growth factor mediated cells that proliferate during the growth and repair of neurones.
Perhaps the copper element of the normal healthy prion protein plays a role in the balance and conduction of electromagnetic pathways - the pathways which distribute the energy of UV throughout the body.
In this respect, it could be said that the discovery of the function of the prion protein may turn out to give further scientific substance to the existence of the electromagnetic meridians recognised by Chinese medicine - where the healthy copper prion performs a regulatory role in maintaining the electro-homeostatis at the acupuncture nodes and along the meridians.
Copper prions as the conductors / manganese prions as the blockers of electromagnetic energy flow.
The fact that copper is employed in electric wiring manufacture for conducting electric currents, whereas manganese is employed in the manufacture of batteries / Light bulb filaments for storing up electrical energy, may well elucidate a possible overall explanation for the cause of prion diseases; where the healthy copper prion protein serves to conduct the vital electro-energy of sunlight along the circadian pathways in the brain - in order to help propel the sleep. sex, behavioural, growth and immune response cycles, etc., whilst the aberrant manganese contaminated prion serves to block and store up that UV derived energy to a critical explosive ‘flash point’ ; a level which detonates off neuropathogenic cluster bombs of free radical chain reactions throughout the circadian pathways of the brain .
In this respect, the oxidative impact of UV energy received at the retina will no longer be quenched / dissipated due to the absence of normal copper prions. Instead, the electromagnetic energy flow piles up, and finds itself absorbed by the abnormal accumulated stores of manganese prions. The energy is subsequently misappropriated into converting the abnormal accumulated store of manganese 2+ prions in the retina into its highly reactive manganese 3+ or 4+ prooxidant prion forms ? So any accumulations of manganese prion proteins in the retina will find themselves switched from a safe to lethal form.
Does the oxidising effects of UV therefore serve to unleash a kind of ‘ Dr Jekyll and Mr Hyde’ like capacity of the prion protein in the manganese contaminated / copper depleted mammal; which, in turn, kicks off a whole chain reaction of free radical mediated assault on the central nerves ? Whence, a neurodegenerative ‘melt down’ of neurones proliferates, and TSE ensues ?
The new strain TSEs and the modern day cocktail of eco-oxidizing agents
Having considered environmental factors responsible for the genesis of traditional TSEs, what new factors can be held accountable for the more aggressive modern day strains of TSE ( BSE, vCJD ) surfacing in younger mammals ? Perhaps these ‘rapid attack’ new strain TSEs could result from our increasing modern day exposure to the more potent oxidizing effects of a cocktail of man made environmental agents which can penetrate the central nerves - such as the systemic organophosphates (head lice shampoos, warblecides, etc ), radar, ozone, increased UV (due to stratospheric ozone depletion), microwave mobile phones, infrasound ( from Concorde’s 100 km boom carpet of supersonic waves ) etc, - thereby serving as the lethal oxidative trigger that produces a more virulent, accelerated version of TSE; with full blown symptoms erupting in much younger mammals than normal.
TSEs could therefore be viewed as diseases that result from a breakdown of oxidative homeostatis within the organism ; where TSE susceptible mammals living in environments that are concurrently challenged by high intensities of manganese and oxidising agents, and by low levels of antioxidant metals (Copper/ selenium/ zinc ) which all combine to create circumstances where the central nerves are severely hyperoxidized - thereby kicking off free radical chain reactions that can efficiently proliferate in organisms lacking antioxidant defence.
The pattern of emergence of both traditional and new variant CJD clusters in rural/coastal areas as opposed to urban areas substantiates this idea of an oxidative origin hypothesis well. Furthermore, the predominance of CJD cases erupting in rural/coastal areas helps to dispel the myth that vCJD arises from ingestion of BSE affected beef products - meat products being consumed equally by urban and rural populations alike.
Rural / coastal areas have become increasingly exposed to a toxic cocktail of oxidizing agents, such as UV, infrasound, ozone or systemic crop sprays over recent years; whereas town environments have ironically been spared. This is largely due to the shield of smog which envelopes the majority of urban airspaces and serves to scatter and absorb the incoming UV rays; thereby preventing the deadly UV - exhaust gas interaction, with its deadly consequence of ozone formation.
All of this helps to explain why rural residents are amongst the highest risk group for developing CJD.
It is perhaps no surprise that the oxidative environs of Staten island and Long island in the USA - both under the take off flight paths of JF Kennedy airport - ( enduring an oxidative cocktail of Concorde take offs, radar, coastal UV / ozone, microwaves, etc ) has demonstrated by far the highest incidence cluster of CJD in the USA .
Manganese breaketh Man.
The high level manganese connection to the epidemic of the new variant TSE correlates as convincingly as the eco-oxidative connection. 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; as free access mineral licks, tablets, fertiliser and fungicide sprays, paints, petrol additives, etc. Or via increased consumption of trendy food products such as soya which naturally bioaccumulate high levels of this metal from the soil.
Disturbingly, manganese is added to artificial milk substitute powders for calf and human infant consumption at about 1000 times the levels found in normal cow and human breast milk respectively. Excess intakes of dietary manganese poses a great risk when fed to the immature mammal, since the homeostatic regulatory mechanisms of the blood brain barrier are underdeveloped at this stage, thereby permitting an excessive uptake of manganese and other metals into the brain.
The addition of manganese to artificial milk powders probably explains why dairy cattle - who were invariably reared on this milk powder - suffered such a high incidence of BSE, whereas beef suckler and organic cattle - who were invariably reared on natural cow’s milk - suffered zero BSE incidence.
Some would question how the toxic manganese-oxidant theory of TSE origins can account for the well recognised ‘iatrogenic’ forms of TSE, where growth hormone treatment of humans - which utilises pituitary tissue as the inoculant - can lead to a form of CJD.
But intriguingly, tissues such as pituitary and retina which transmit TSE in the lab most efficiently, are the precise same tissues in which manganese concentrates most intensively. Could the high manganese levels contained within these tissues act as the so called infectious agent ? particularly once the metal has been oxidized into its lethal prooxidant 3+ form ?
Despite the apparent reluctance of Establishment bodies to overtly address the raft of hard evidence amassing around the manganese - oxidant theory of BSE causation, we are still gaining positive ground. But funding has not been forthcoming, despite recommendations by the Uk’s BSE Inquiry report, etc, as well as MAFF’s subsequent invite asking me to resubmit proposals for research along these lines. Such a negative dismissal has impaired the whole healthy evolution of this important new perspective on TSEs. Furthermore it has blocked the development of a possible cure for new variant CJD.
In the light of recent Frence and other Euro threats to sue the UK for allegedly giving them BSE- vCJD, it is puzzling to witness the continuation of the dismissive mindset of UK authorities towards any evidence that backs environmental involvement in TSEs; unbelievable , in fact, after studying Professor Bounias’s recent paper which highlights the exact same spatial-temporal correlation between warble fly insecticide use and BSE emergence in France, as observed in the UK .
To the Ends of the Earth.
Meanwhile, I have continued to expand my field investigations by designing a full scale environmental surveillance programme( metal and oxidant analyses, etc ) of relevant water, soil, vegetation, atmosphere, blood / tissues that will be exercised in the variant CJD and BSE clusters that have recently erupted across the UK and Europe.
I have also been invited to study a cluster of mystery progressive, fatal neurodegenerative disease ( known as Birds disease ) that has erupted amongst Aboriginal and Caucasian people thriving on a remote island ecosystem off the Northern Australian Coast - Groote Eylandt. The problem first developed after a mining corporation started the open cast mining of manganese on the island in the 1970s. A fine black manganese dust has reportedly coated the entire island.
True to form, the local authorities have seemingly scapegoated the emergence of this syndrome - which manifests as a motor neurone disease or a mystery dementia - onto a rare virus that was introduced by a Portugese miner who came to work on the island three decades ago.
With permission from the local Aboriginal society, I hope to acquire brain sections from those who have died of the TSE-like ‘dementia’ strain of this disease and see if the archetypal TSE “prion” tombstone features can be detected.
I have also managed to persuade a local GP in Darwin to treat some of the early stage victims of ‘Bird disease’ with the manganese chelating drug; EDTA ; Up until now, victims of this grotesque disease have been kept in total dark regarding the existence of a possible cure and escape from what has always been considered to be an inevitable death. But today, the treatment has just begun.