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QUESTION 1.
The pathology of the copper deficient brain is completely different from
the pathology of TSE diseased brain, so how can you claim that copper
deficiency is linked to the cause of TSE ?
ANSWER
People get me wrong - my thesis promotes a multifactorial aetiology
involving a combination of factors. I am saying that sporadic TSEs are
essentially trivalent manganese toxicity on top of subclinical copper
deficiency, so you would get an entirely different pathological profile
than what you would observe in straight Cu deficiency. For instance, the
classic Mn toxicity hallmarks such as amyloid fibrils, neuronal loss,
astrogliosis and shrunken basal ganglia (caudate nucleii, putamina). are
precisely present in TSE neuropathology.
Most normal prion proteins bond onto five copper atoms per molecule in
the healthy individual; but the different strains of scrapie are largely
dictated by the number of copper atoms that bond to prion protein. Some
TSE susceptible genes only encode for synthesis of prion proteins that
will bond 3 copper atoms; thus predisposing that mammal to scrapie
susceptibility which will take some time to incubate, etc, etc.
On the other hand, the copper deficit in the more aggressive, short
lived BSE and variant CJD syndromes is not caused by primary copper
deficiency due to environmental deficiencies , but is caused by certain
organo pollutants such as systemic insecticides (eg OP warble fly
chemicals , which actually directly modify the histidine ligands
(via generation of singlet oxygen) which bond copper to the prion
protein. So basically, no copper can bond to prion protein any longer;
whether copper is abundant in the brain or not! This is why vCJD/BSE is
so much more rapid than traditional scrapie, simply because no
copper can bond at all; whereas the more protracted incubation period in
sporadic TSEs, such as scrapie, is genetically mediated by a maximum of
only one, two or three copper atoms being able to bond to the prion
protein - thereby creating the scrapie susceptible genotypes where
susceptibility is activated once environmental copper becomes deficient
QUESTION
- Your theory claims that organophosphate chemicals used to
kill warble flies on cattle underlies the cause of BSE. However Guernsey
island had the highest incidence rate of BSE in the world, yet never
encountered a problem with warble fly infestation. Please explain this
stumbling block to your theory?
ANSWER - This is a very good point, but I would say that the same
types of systemic dithiophosphate OPs used for warble fly control in the
UK, were actually used regularly on Guernsey (albeit at lower doses)
for the control of cattle lice; since lice breed efficiently in the warm
winter maritime climate of Guernsey island.
Furthermore my theory on the cause of BSE is multifactorial - eg; it
advances a mix of genetic and environmental causal factors. And it is
the copper-chelating property of the systemic dithiophosphate
insecticides that constitutes just one of the dirty detonators for
increasing susceptibility to BSE. These chemicals deprive the copper
supplies in the brain of the treated cow thereby starving the
prion protein of its copper component - vital for healthy brain function
and for dealing with electromagnetic pollution of the brain cells .
Copper starvation renders prion protein susceptible to manganese
replacement - and manganese was added to calf milk powders / cattle
feeds / mineral formulations at the same concentration on Guernsey as in
the UK; since all Guernsey livestock feeds were being imported from the
UK during the BSE period. So both Guernsey and the UK shared the same
feeds.
It is fair to say that the lower doses of systemic OP used on Guernsey (relative to the UK) would simply have been insufficient to cause the
high rates of BSE recorded there. But when you consider the additonal
facet of the well renowned copper deficiency in Guernsey's native
granitic soils, this compounds the problem of OP chelated copper ;
resulting in overall copper deficiencies in cattle on Guernsey that
could be sufficient to account for such high rates of BSE there.
Furthermore, my final BSE prerequisite of high levels of electromagnetic
radiation is well fulfilled in the Guernsey island context. The
naturally high coastal levels of ultra violet radiation, ozone, radar,
etc coupled to the intensive levels of infrasonic shock waves from
the Frence Supersonic passenger aircraft accelerating/decelerating
directly overhead every day, puts Guernsey in the upper league as far as
electromagnetic exposure levels go!
QUESTION 2. Organo phosphate (OP) chemicals were used to control
livestock parasites in countries all over the world, yet the BSE
epidemic was virtually confined to the UK. If OPs were the cause, then
why hasn't BSE erupted all over the world?
ANSWER; The lynchpin of the 'OP prerequisite' in my BSE origin theory
hinges on the fact thatthe UK was unique in using a ' systemic' class of
OP insecticide at twice the dose rate compared to the rates used in the
few other countries in the world who used systemic type formulations on
their cattle. So Britain was the only country in the world to compel
twice annual usage of a 20% concentrated systemic formulation of
dithiophosphate at a 20 mg/kg body weight dose rate. The few other
countries who used the systemic type, applied the chemical at a 10 mg/kg
dose rate for lice control, and even then on a voluntary basis only.
Africa and other third world countries used OPs frequently , but these
were invariably applied as 'non systemic' dips , baths and powder
formulations which were not designed to kill internal parasites like the
warble; therefore were not designed to travel through the skin and
contaminate the central nerves - eg where BSE pathogenesis originates.
Australia and New Zealand, which has remained totally BSE free to date,
has never had a warble fly problem. BSE free USA /Canada does have a
small ongoing warble problem but has always wisely resorted to using
much less concentrated solutions of non systemic OP for fear of
contaminating the milk of the treated cows. Doses as low as 2mg/kg body
weight are not uncommonly used out there - nearly 10 times less than
that used in the UK!
But when Japan recently started to use systemic OPs on a few of their
herds (in North Hokaido) that were importing in warble infested cattle
from N America, three of those herds had BSE breakdowns.
It is interesting that BSE seems to have erupted in other European
countries following a remarkably similar spatial/temporal way in
which those countries had adopted compulsory warble control.
Compulsory warble treatment with the high dose systemics has only taken
place in the UK (largely between 1980 and 1996), but Switzerland,
Ireland, and the Britanny areas of Europe had been running similar
warble campaigns from the 1980s onwards - albeit with only once yearly,
lower doses of OP. But ten to twenty years later we had a situation
where the whole of France as well as other European countries such as
Portugal, Spain, Italy, etc, have joined up with the Euro
"COST" warble eradication campaign; and now they too have an
emerging BSE problem.
My studies have shown that the further BSE prerequisite of
"addition of manganese in feeds" is also present in all of the
intensively farmed areas of Europe that have encountered endemic BSE
problems to date.
Mark
Purdey
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