Mad
Cows or Mad Science?
Insecticide-created
rogue prions may
cause BSE and CJD
by
Fintan Dunne
Tel: +353-87-6814-133
Editor,
AidsMyth.com
Research
Kathy Mc Mahon
7th
December 2000
"The media loved the theory because
they could drum up a viral holocaust-horror scoop.
The vegetarian and green lobbies found themselves landed with a powerful
propaganda weapon on their plate— turning cows into cannibals. And the
UK scientific establishment could go on drawing generous grant funding
for their viral witch-hunt without the embarrassment of having to account
for years of barking up the wrong tree. And then the government could
foist the blame of BSE onto a naturally occurring agent for which no significant
vested interest or official body could be held accountable."
-Scientist, Mark Purdey.
As
Europe prepares to mass-sacrifice cattle on the altar of consumer protection,
convinced that infectious prions from BSE cattle cause neurodegenerative
CJD in humans, marginalised
scientists have evidence that both diseases are environmentally
induced, rather than infectious.
Despite being rejected by mainstream consensus, the alternative
scientists claim that prions damaged by insecticides interact with manganese
in animal feeds. Their research examines how organophosphate insecticides
-such as Phosmet used in high doses in British warble fly dosing- may
turn prions 'rogue.'
The
alternative theory matches the epidermiological spread of clusters of
CJD in humans and the incidence of BSE-type diseases in animals. If the
research is valid, then not only is the EC action futile, but some lotions
for scabies and head lice could be priming humans for CJD susceptibility.
Cambridge University neurodegeneration scientist,
David R. Brown is dismissive of what he terms "a very limited amount
of science by a few." He insists there is "no evidence an infectious
agent is present in either meat or milk."
"Simple tests on udder walls of cows --which could easily detect
the infectious prion-- have not been done, why I don't understand."
His latest published study examined how organophosphate(OP) in systemic
warble fly insecticide can deform the prion molecule, rendering it ineffective
at buffering free radical effects in the body. Worse still, the prion
is then partial to bond with manganese and become a 'rogue' prion. A chain
reaction whereby rogue prions turn others to rogues also, can explain
the bovine spongiform disease mechanism.
He showed how prion molecules bond benignly with copper, but toxically
with magnesium when the prion is degraded by OP effects. Natural variations
in relative environmental availability of manganese versus copper would
also trigger the prion degradation.
Organic dairy farmer and peer-published independent scientist, Mark
Purdey, says the accepted theory of transmission from BSE-infected cattle
to human CJD by bonemeal or meat is dependent on a mutant prion that has
never been isolated under the scientific protocol called Koch's postulates.
Purdey's insistence on sticking to the letter of this scientific
law earned him the condemnation of UK officialdom when he first mooted
his theory. But Purdey pointed to CJD clusters downwind of a British Phosmet
production plant to back his case.
He gave evidence to the UK Government BSE inquiry and was supported
by Conservative MP, Thessa Gorman. His views were discounted, but his
subsequent research has confirmed the alternative theory. Despite this
he was denied even exploratory funding.
Speaking
from his Somerset farm today, to AidsMyth.com, as plans for the European
cattle cull forge ahead, he asks "why is it that CJD degeneration
in humans begins in the retina, and that CJD disease clusters are found
in high altitude locations?"
The question is rhetorical, and Purdey has an eye-opening answer.
He
argues that the prion molecule
has a natural role as a shock adsorber of damaging energy from ultraviolet
rays and other oxidizing agents.
Once the prion defence system is rendered ineffective by organophosphates
in human head lice lotions, these harmful effects can accumulate. Eventually,
UV radiation damages the retinas and oxidative stress destroys the brain
tissues of CJD patients. This theory would predict higher CJD incidence
in mountain regions where UV radiation levels are elevated. That prediction
holds true.
A similar but accelerated mechanism could be driving BSE. ICI's
Phosmet warble fly insecticide -applied on the backs of animals along
the spinal column, similarly degrades prions. "Systemic versions
of the insecticide are designed to make the entire cow carcass toxic to
warble fly," explains Purdey. "Unfortunately it's toxic to prions
too -especially those prions located just millimeters from the point of
application."
The damaged prions are now ready to react with manganese in animal
feed or manganese sprayed on land -to become the driving force of the
BSE degeneration. Purdey
says manganese-tipped prions set off lethal chain reactions that neurologically
burn through the animal.
Chickens notoriously
excrete most of the supplements fed to them -including manganese. And
their manganese-rich excreta have been blended into cattle feed in the
UK. Natural variations in the relative environmental availability of copper
and manganese can also spur prion degeneration says Purdey.
If these disease mechanisms are valid then there is a significant
risk attaching to the use of organophosphate in humans. Preparations for
head lice and scabies are known to be overused in practice and might be
priming users for CJ disease.
Purdey believes his bias for field work is the key to his success.
He bemoans the "reductionism" of much lab-centered science.
"I have traveled the world to investigate known clusters of spongiform
disease -something mainstream researchers don't seem remotely interested
in doing."
Since first postulating an environmental -rather than infectious-
theory of spongiform diseases, Purdey has built evidence from
around the world that explains
and predicts the incidence in humans and animals: a cluster of CJD in
Slovakia, Eastern Europe -around a manganese plant; Icelandic reindeers
with BSE who were found to be eating pine needles rich in manganese; the
futile slaughter of sheep in Cyprus -only for BSE to reemerge within years.
"The reappearance of BSE in Cyprus obviously points to an environmental
cause," says Purdey, who is sanguine when reflecting on the condemnation
of him by mainstream scientists.
"I suppose they have mortgages and kids who need to go to university,"
he muses. "Privately, some were agreeing with me, but then they would
denounce me publicly. It was quite strange really."
Critical
scientists like Purdey are unlikely to prevail in this argument. The pharmaceutical
industry holds most research purse strings and would hardly energetically
explore an avenue of research that could expose them to litigation as
the prime cause of BSE. The official theory is lavishly funded, alternative
theories rarely, if at all.
There are even more explosive implications to the new work. Purdey
says similar OP-induced protein deformation could also underlie Alzheimer's
disease. If that were true, the litigation fallout would destroy some
pharmaceutical giants, and a lot of very influential noses would be out
of joint.
Disturbingly, Purdey and other brain researchers seem to have had an undue
share of unfortunate accidents. Purdey's house was burned down and
his lawyer who was working with him on Mad Cow Disease was driven off
the road by another vehicle and subsequently died. The veterinarian on
the case also died in a car crash.
Dr. C. Bruton, a CJD specialist -- who had just produced a paper
on a new strain of CJD -- was killed in a car crash before his work was
announced to the public. Purdey speculates that Bruton might have known
more than what was revealed in his last scientific paper.
In 1996,
leading Alzheimer's researcher Tsunao Saitoh, 46 and his 13 -year-old
daughter were killed in La Jolla, California, in what a Reuters report
described as a "very professionally done" shooting.
What all of these have in common -- Alzheimer's Disease, Mad Cow
Disease, and CJ Disease -- is abnormal brain proteins and a putative link
to organophosphates. Even Gulf War syndrome among returning veterans has
been attributed in part to the insecticide. But the sidelined scientists
suspicions are still largely ignored.
In their favour at the moment, is a growing unease on the part of
the public. As BSE forges on and Governments panic, Science may be out
to lunch on BSE, compromised by bovine spongythinking myopathy.
Copyright ©
2000
www.AidsMyth.com_
REFERENCES
& SOURCES
by Mark Purdey:
Animal Pharm
http://www.westonaprice.org/myths_truths_mad.html
UDDER MADNESS!
http://www.schnews.org.uk/archive/news252.htm
Theories of
Mad Cow Disease
http://www.mad-cow.org/~tom/spiroplas.html
Mad Cows and
Englishmen
http://www.oneworld.org/news/reports/apr96_bse1.html
Intrigue, Scientists
and Mad Cows
http://www.vaccines.plus.com/madcow-update1.html
OTHERS
UK Farmer says
chemicals cause BSE
http://news6.thdo.bbc.co.uk/hi/english/uk/newsid_72000/72866.stm
UK BSE papers
to be published on the Net
http://news6.thdo.bbc.co.uk/hi/english/uk/newsid_63000/63794.stm
Blood donations
to be treated against CJD
http://mad-cow.org/~tom/leuco.html
Update on animal
brain disease from
British dairyman/researcher Mark Purdey
http://www.profarmer.com/newsroom/followup/purdey.cfm
Review of warblecide
epidemiology
http://www.cyber-dyne.com/~tom/warble.html
BSE
BSE Inquiry Statements of Mark Purdey
23 March 1998
http://www2.prestel.co.uk/littleton/ek3_purdey_023.htm
Issued 07/06/1999 (not scheduled to give oral evidence)
http://www2.prestel.co.uk/littleton/ek3_purdey_023a.htm
Issued 12/01/2000
[12th Jan 2000 - RW]
http://www2.prestel.co.uk/littleton/ek3_purdey_023b.htm
THE BSE INQUIRY
http://www.bse.org.uk/transcripts/tr980402.txt
Introduction
http://www.vegansociety.com/info/info03.html
The Organophosphate-BSE
Hypothesis and CJD
http://www2.prestel.co.uk/littleton/ek3_ops_bse_cjd.htm
The important
unofficial organophosphate site.
http://www.mapperleyplains.co.uk/oprus/
"MAD COW"
DISEASE IN BRITISH SHEEP?
http://www.linkny.com/~civitas/page75.html
PROPERTIES
OF ORGANOPHOSPHATES.
http://www2.prestel.co.uk/littleton/ek3_wheatley.htm
The Official
Mad Cow Disease Home Page
http://mad-cow.org/
Premature Sexual
Maturation of Human Children
http://www.trufax.org/research/f40.html
ProMED Digest
http://id.medscape.com/other/ProMED/1996/apr/ProMED.V96.n083.html
SUPPLEMENTAL INFORMATION:
Edited Introduction to the Purdey hypothesis
on Spongiform Encephalopathy (SE)
The main problem we have with the meat and bonemeal (Mbm) hypothesis of
either MAFF or the Royal Society is the amount of scientific contra evidence
that exists to them. Any hypothesis that can’t demonstrate Koch’s postulates
after 15 years of international multi million pound research should be
jettisoned.
Mbm fed to experimental animals does not produce SE
Millions of tons of Mbm exported abroad, when mutant prion material was
at its highest, did not produce any BSE.
Mutant prion has been drastically reduced (to presumably nil) in Mbm over
the last 14 years and yet BSE has been starting, with a continued trend
upwards, in a number of EU countries ie Ireland, Portugal, Belgium, Brittany,
Switzerland.
The hypothesis in summary:
In prion disease there is an error in the manufacture of the prion protein
caused by an abnormal configuration and or binding of two key metals Copper
(Cu) and Manganese (Mn). Mn substitutes for Cu when the latter is low
or fails to bind to the histadine sites of the octapeptide repeat region
of the protein. This substitution results in eventual conformational change/
protease resistance . In addition the host would be exposed to a free
radical trigger that generates excessive oxidative stress and up regulates
the prion protein as a defense
The most important function of the Prion is to resist oxidative stress
by acting as a Super Oxide Dismutase (SOD). On conformational change the
prion cannot function as a SOD and protect cells, and consequently a pro
oxidative status quo is established at a location in the host .This pathology
spreads through the host during the incubation period, with neurones eventually
being destroyed by the build up of toxic by products such as hydrogen
peroxide, quinones or peroxynitrite.
Finally the metal species bound by the prion is more highly oxidised ie
Mn 3+ or 4+ and this may explain strain difference and difference in incubation
times. Environmental factors that affect the levels of metals ,their species
and protein ‘sinks’cause the disease. Oral infectivity via food products
is secondary and we think is rare in vivo. The often quoted transmission
experiments are not reliable predictors of the situation in life - even
oral homogenate studies are unreliable because reactive metals are freed
from protein sinks in the process.
Further reading: Mark Purdey ’Ecosystems supporting TSEs demonstrate excesses
of the pro-oxidant Manganese’ Medical Hypotheses (2000) 54 (2) I’m hoping
to get this online soon. D.R Brown et al ‘Consequences of Manganese replacement
of Copper for prion protein function and proteinase resistance. EMBO journal
vol 19 no.6 p 1180 - 1186 Useful background New Scientist 26 august 2000
article ‘Metal Heads’ by Jonathan Knight
FAQ ; Organophoshates (OPs) and TSEs: The OP Phosmet used at 4 times the
recommended max dose on cows in Britain in the 80s to control warble fly
is a di thiophosphate systemic OP. The 2 sulphurs bind to copper forming
a mercaptide ring. The Institute of Psychiatry conducted trials adding
this OP to living cell cultures at very low dose. Off the record we were
told that phosmet had created a conformational change in prion protein
.This part of the work was suppressed by SEAC and not published or presented
to the BSE inqiry.
Some OPs contain Mn - Mancozeb, Maneb. Mn is often sprayed on farmland
where Mn levels are low. OP residues increased in Mbm in the early 80s.
Our current studies: Scrapie in Sardinia , TSEs in Calabria , vCJD (Kent,
Queniborough, Armthorpe ) - We receive no funding for these.
Past studies: Rida in Iceland, CWD in Colorado , CJD in Slovakia , Scrapie
in Somerset/ N.Devon
Urgenttly needed, but straightforward, Lab research :
Identify what is bound to the histadine sites of the octapeptide repeat
in BSE, CJD and Scrapie prion material.
Phosmet + live cell culture, transmit the result
Maneb + live cell culture, transmit result.
High Mn and low cu in transgenic mice.Transmit
Trial therapeutic strategies:
1)Desferrioxamine 2) Porphyrins 3) Atropine/ oxime.