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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 / researcher
Mark Purdey and his original field investigation which ran in tandem
with the laboratory quest of Cambridge biochemist Dr David Brown to
unearth the truth underpinning the original cause of these grotesque
diseases.
Hard evidence so far amassed by Brown and Purdey�s research
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 notion
continues to accumulate momentum, a radical upheaval of the status
quo mindset can be expected.
Despite their appealing story of discovery generated from the
combined, lateral perspectives of field and laboratory studies,
their published works have largely been dismissed and 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 various 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 insecticide in relation to the few countries who used
this type of insecticide abroad.
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.
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, 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 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 TSE ( Transmissible Spongiform
encephalopathy ) susceptible 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 of the relevant TSE affected
species 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 factories,
lead-free petrol refineries, etc
Purdey�s observations lead him to 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.
His lab studies were complementary to Purdey�s field studies; thereby
providing 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 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 that had died of
natural causes.
copyright 2002 by Mark Purdey All Rights Reserved
