<Mark asked me to forward this just updated version of the earlier post before discussion commences. Folks PLEASE dig deep and ask Mark any questions you have about his thesis or surface any weaknesses that you see in it. Only by working together in matters like this can we hope to restore some level of safety to the industrial food system. It's not something any of us can feel separate from, as either producers or consumers. Furthermore, seeing the government and the corporations destroying herds and farms to cover their own tracks is somethint no reader of this list should stand for. It will happen again and again, unless the electorate realizes that that the grassroots they tromple on will stand for no more. -Allan>
EDUCATING RIDA (Rida is the Icelandic for transmissible spongiform disease) - An underground scientific journey into the origins of spongiform disease. by Mark Purdey. Background. Since 1986, the infamous novel neurodegenerative syndrome , BSE and vCJD , has insidiously blighted the heartbeat of British Agriculture. 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 the eco-detective escapades of maverick farmer /spongiform researcher Mark Purdey and his original field investigations which ran in tandem with the laboratory quest of Cambridge Uni biochemist, Dr David Brown. Their work has gone a long way towards unearthing the truth underpinning the original cause of these grotesque diseases. Hard evidence amassed by Purdey�s research so far, indicates that vCJD and BSE could both result from separate exposure of bovines and humans to the same set of toxic environmental factors; 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 appealing story of discovery generated from the lateral perspectives of both field and laboratory studies, Brown and Purdey�s published works have largely been dismissed, with all funding proposals irrationally rebuffed at peer review. Contrary to the recommendations to UK government by the 1999 BSE Inquiry report, rejection of Brown and Purdey�s grant proposals continues to present day, including one submission aimed at developing a feasible cure for vCJD ! The Lone Voyager Mark Purdey first came to the fore when he successfully quashed the UK government�s compulsory warble fly eradication regime in the high courts in 1984. This exempted him from treating his 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. Purdey was therefore not surprised to witness BSE rearing its ugly head in the UK cattle herd in 1986; which, in his 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 were applied in the few other countries who used this type of insecticide. Purdey was a working dairy farmer with first hand experience of BSE erupting in cattle that had been purchased into his organic farm. He 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, Purdey 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. But it did seem possible that MBM played a role in the spread of the BSE agent from cow to cow, where feeding/recycling of BSE affected cow brain back to cows, caused the disease agent to bioaccumulate - much like infamous DDT insecticides - up through the bovine food chain. The Flaws in the Conventional Hypothesis. Purdey cites the following flaws which indicate that MBM / BSE beef could not have served as the all-important single causal factor in the origins of BSE/vCJD; 1. Thousands of tons of the incriminated MBM feed was exported for cattle feed during the 1970s/1980s 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 straight form or as an ingredient of 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, enabling the �agent� to jump across into cattle, thereby 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 remained BSE-free. 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 BSE. 5. There have been no cases of BSE in the other TSE-susceptible (Transmissible Spongiform encephalopathy ) ruminants such as goats and sheep despite the customary inclusion of a MBM protein source in their feeds. 6. Four of the original five kudu antelope that developed BSE at the London zoo had had no possible access to MBM containing feeds. 7. 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 any resort to feeding concentrated feeds at all. Yet BSE struck down four animals on this holding. 8. The UK�s mechanically retrieved meat products / baby foods blamed for causing vCJD were exported all over the world to countries where vCJD has not erupted. 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. 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. 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. Purdey 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 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, Purdey eventually raised 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. So Purdey went back to square one assuming that OPs , in combination with a further factor X, could fulfill the final missing link. The Cluster Buster Purdey grew 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. He embarked upon a refreshing global trek to analyse the unique environments where traditional TSEs had erupted as high incidence clusters for many years. He tramped the most clearcut cluster zones in Colorado, Iceland, Slovakia, Calabria, Sardinia, etc, where an assortment of animals and humans had developed TSE at exceptionally high incidence rates. Abnormally high levels of the metal manganese, and rockbottom levels of copper, selenium and zinc were measured in all of these food chains in common. Levels returned to normal in disease free areas adjoining. The Men from Manganese. A specific environmental source of manganese could be pinpointed in each cluster zone; where habitats 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 ,volcanic, acid rain, steel/ glass/ ceramic /dye/munitions factories, lead-free petrol refineries, the take off airspace beyond airports, etc. Purdey�s observations caused him to construct a holistic hypothesis on the aetiology of TSEs, which lead him to connect with the pioneering laboratory studies of Dr David Brown at Cambridge; an extensively published biochemical genius who had single mindedly 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 Purdey�s field studies; thereby providing the other half of the neccessary ground work on which Purdey devised a hypothesis proposing that manganese could substitute itself at the vacant copper site on the prion protein; this aberrant substitution occurring in susceptible mammals who are entirely self sufficient upon high manganese / low copper foodchains. Purdey proposed that this 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 David Brown�s team and a Frence team undertook 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 transition metal, �silver�, which like manganese, will also readily substitute at copper ligands on prion proteins . These environments were 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 Purdey�s trek took him to a newTSE hotspot, he found himself face to face with the same type of high altitude, snow covered, pine tree terrain. Putting aside the common high manganese / low copper connection, this common geographical association with TSE cluster regions continued to baffle him; each time he arrived at a fresh TSE location he found himself recounting the memory of the first glimpse of chronic wasting countryside of deer and elk in Colorado- the snow peaked Rocky Mountains sawtoothing the july skyline beyond the parched out Denver Plain. 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 hideous bright white concrete sections - unusual for this area. All were couched within a sun parched, glaring landscape of bare white sandstone, producing all the prerequisites required for a most intensive ultra violet (UV) hotspot location; immediately connecting Purdey to the well recognised �high UV� nature of high altitude, snow covered, coniferous tree terrain which he had found in common in the Icelandic, Colorado, Slovak cluster ecosystems under study; areas also connected to the oxidizing effects of high levels of atmospheric ozone generated by the interaction of UV on the terpine haze exuded from pine trees. 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 or the eyelid or skin of the affected mammal - external areas having front line exposure to sunlight . Plus the fact that the normal , healthy form of copper bound prion protein is located in the circadian pathways which conduct the electromagnetic energy generated by ultraviolet light around the brain - eg , the retina, pineal gland , visual cortex, hypothalamus, pituitary, brain stem, etc. Prion protein is expressed in other tissues of the body which are also involved in the network that conducts electromagnetic energy; for instance in the spleen, lymphatic system, glial cells and nerve growth factor-mediated stem cells that proliferate in the growth and repair of neurones. In this respect, it could be said that the discovery 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 along these meridians. Copper prions as the conductors / manganese prions as the blockers of electromagnetic energy flow. The fact that copper is employed in industrial contexts of electric cable manufacture for conducting electric currents, whereas manganese is employed for storing up electricity in batteries / Light bulb filaments, may well help elucidate a possible overall explanation for the cause of prion diseases; whereby the healthy copper prion serves to conduct the vital electro-energy of sunlight along the circadian pathways in the brain in order to propel the sleep. sex, behavioural cycles, etc., whilst the aberrant manganese contaminated prion serves to blockade and store up that UV derived energy to a critical �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 due to the absence of normal copper prions. Instead, the energy flow will be blocked and misappropriated into converting the abnormal accumulated store of manganese ( both manganese and prion protein tend to accumulate in the retina ) from its innocuous manganese 2+ antioxidant form into its lethal manganese 3+ prooxidant form ? So any accumulations of manganese abnormally attached to the prion protein in the retina will find itself switched from a safe to lethal 3+, or even 4+form. Does the oxidising effects of UV therefore serve to unleash a kind of lethal � 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 Variant TSEs and the modern day increased eco-oxidative assault. This has explained the genesis of the traditional strains of TSE. But what about the causes of the much more aggressive modern day strains of TSE ( BSE, vCJD ) surfacing in younger mammals ? Perhaps these rapid attack neurodegenerations could result from our increased modern day exposure to the more potent oxidizing effects of a cocktail of man made environmental agents which 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, Concorde�s 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 concurrently characterised by high intensities of manganese and oxidising agents, and by low levels of antioxidant metals (Copper/ selenium/ zinc ) combine to create circumstances where the central nerves are hyperoxidized - thereby kicking off a free radical chain reaction that can freely proliferate in the absence of antioxidant defence. The pattern of emergence of both traditional and new variant CJD clusters in rural/coastal as opposed to urban areas substantiates this idea, as well as helping to dispel the myth that vCJD arises from ingestion of BSE affected beef products - products that are 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, 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 airspace which scatters and absorbs the incoming UV rays; thereby preventing the deadly UV - exhaust gas interaction, which yields the deadly oxidant; ozone gas. Manganese breaketh Man Furthermore, the well renowned chronic exposure of village communities to the oxidative assault of agrichemical spray drift, manganese based fungicide and fertiliser sprays, etc, all serves to place the English village community at the top of the league as far as toxic oxidant exposure goes.; thereby placing rural residents 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 ( enduring an oxidative cocktail of Concorde take offs, radar, coastal UV / ozone, microwaves, etc ) has served to host by far the highest incidence cluster of CJD in the USA . The high manganese connection to the epidemic of the new variant TSEs can be just as well correlated as the oxidative connection. Over the last two decades, increased amounts of straight and chelated forms of high concentration manganese oxide additive have been introduced into the bovine, human, pet and zoo animal food chains /ecosystems in Europe - as free access mineral licks, tablets, fertiliser and fungicide sprays, paints, petrol additives, etc. Most 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 manganese poses a great risk when fed to the immature mammal at a time when the regulatory mechanisms of the blood brain barrier are underdeveloped, thereby permitting an aberrant, high rate uptake of manganese and other metals into the brain. 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 ), etc, can lead to a form of CJD. But intriguingly, tissues such as pituitary and retina that are considered to transmit TSE most efficiently, are the exact same tissues where manganese is recognised to concentrate 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 ? Future Pathways. Despite the apparent reluctance of Establishment bodies to overtly address the works of David Brown and Mark Purdey, both individuals independently strive to take this theory to its final conclusive stages. But funding has not been forthcoming, despite recommendations by the Uk�s BSE Inquiry report, etc, as well as MAFF�s subsequent invite to Purdey to resubmit proposals for research along these lines. Such a negative dismissal has thwarted 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, a study that David Brown tried to launch last year. 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 work 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, despite lack of any formal funding, Mark Purdey continues to expand his field investigations. He has designed 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 in the UK and Europe. He has 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, Purdey hopes to acquire brain sections from those who have died of the TSE-like �dementia� strain of this disease and see if TSE prion tombstone features can be detected. Purdey has also been instrumental in persuading a local GP 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, more importantly, an escape from what has always been considered to be an inevitable death. But today, the treatment has just begun.
