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July 24,
2002
MAD
COWS OR MAD SCIENTISTS?
THE
SUPPRESSION OF ALTERNATIVE EXPLANATIONS
By
David Crowe
The
smoke and flames from funeral pyres for hundreds of thousands of
British cows are fading into distant memory, but the fear of this
disease affecting livestock or wildlife continues to circulate the
globe.
Most
people do not realize that there is a non-infectious explanation for
Mad Cow disease and other spongiform encephalopathies and chronic
wasting diseases. This is due to the reluctance of scientists, health
and agriculture bureaucrats and most of the media to question a theory
that affects public health once it is active policy.
One
man, Mark Purdey, has turned himself from organic dairy farmer into an
amateur scientist and globe-trotting epidemiologist to doggedly
continue building the major alternative theory.
The
infectious theory of Mad Cow disease not only resulted in the possibly
unnecessary destruction of hundreds of thousands of cows, but it
diverted attention from other causes of health problems facing
livestock and wildlife. It created a fear of eating beef (perhaps not
entirely misplaced, but for the wrong reasons) and resulted in the
circulation of tons of toxic materials from the slaughtered cows into
the atmosphere. It also prevented investigations into alternative
solutions to the epidemic of disease, even though these might be
cheaper, more constructive and far less destructive.
The
dominant belief is that Mad Cow disease (also known as Bovine
Spongiform Encephalopathy or BSE) and the related diseases Scrapie in
Sheep and vCJD (variant Creutzfeldt Jakob Disease) in humans are
caused by a prion, a mutant protein. These semi-living beings are
thought to be able to withstand temperatures that would kill the
hardiest bacteria, viruses and parasites. It is believed that this
allowed them to be transmitted from sheep to cows through the
rendering of sheep brains into MBM (Meat and Bone Meal) protein
supplements for cows.
An
apparently unrelated health problem in cows that existed before Mad
Cow disease was warble fly infestation. These flies lay their eggs in
a cow’s skin, causing health problems and reducing the value of cow
hides. To combat this, in the early 1980’s the British government
mandated the use of heavy doses of organophosphate insecticides. These
were poured in an oil-based liquid along the spinal column of cows. It
was intended that they be systemic, absorbed into the cow’s body, as
it was believed that this was necessary to provide full and enduring
protection from warble flies.
Mark
Purdey was one of a handful of farmers who refused to use
organophosphates (such as Phosmet) on their cows in 1982. He was
concerned that the high doses would damage the health of his cows
because the application was so close to the spinal column. He was also
concerned about the health of people who drank milk from his cows. In
1984, Purdey won his court fight, and gained the right to use less
toxic methods to combat warble fly.
When
the first cases of neurological problems were reported in cows in
1985, Purdey felt that his avoidance of these pesticides had been
vindicated. However, researchers and the British Government had a
different idea, blaming the rapidly emerging disease on the recently
postulated prion, based on the detection of protein plaques in the
brains of sick cows.
Purdey
started to publicly argue his theory that organophosphate pesticides
were actually the cause of neurological problems, attracting some
attention, and seriously annoying the British scientific establishment
and government who were starting to act as if the infectious theory
was fact.
Purdey
noted many inconsistencies in the prion theory. Cows were supposedly
infected by feeding on supplements containing the brains of sheep with
Scrapie, yet Shetland Islanders had been eating potted sheep brains
for centuries without similar diseases occurring. He also noted that
British byproducts were exported around the world, yet the 170,000
British cases of BSE far outnumbered the total in the rest of the
world. Cases of BSE had been found on organic farms with cows brought
in from outside, but not on those raised from birth on the organic
farms, even though organic farming rules allow restricted amounts of
the suspect MBM feeds. Other ruminants, such as goats and sheep, were
not affected by Mad Cow-like diseases in England, even though they
were fed MBM supplements. Conversely, several antelopes at the London
Zoo and cattle at the Liscombe experimental farm developed BSE, but
had never been fed MBM supplements.
When
BSE was found in other countries it was in places like Bretagne in
northwest France where organophosphate pesticides were first
encouraged by the French government. As in the UK, BSE cases first
occurred a few years after the pesticide program was initiated. The
lower number of cases may be due to the lower doses used, the use of
annual treatments (as opposed to twice a year in the UK) and because
the program was not mandatory.
As
further evidence, the decline in BSE cases in the UK began about the
same time the warble fly eradication program ended.
British
cases of vCJD in humans also fit the environmental theory. The disease
was found in some long-term vegetarians and in humans who had never
eaten cow brains. There is no good explanation of why cows could only
get BSE from eating sheep brains, but humans could get it from eating
only other parts of cows.
Although there was a great deal of panic, there were actually few
cases in humans. Purdey noted that about 80% of the 82 cases were in
rural areas, even though more than 80% of Britons live in urban areas.
One cluster in the Weald district of Kent is in a hops growing area
where organophosphate pesticides are used at 100 times average levels
for all crops.
Purdey
lobbied for government funding to test his research. Eventually, he
did get a small amount, and Dr. Stephen Whatley of the University of
London was able to show in a test tube that organophosphates were
found to produce 3 of the 4 protein transformations required to create
the mutant prion protein. A victory, but also a major defeat. The UK
BSE inquiry admitted that "the door is not yet closed on the
possibility that OPs [organophosphates] played a role in rendering
cattle susceptible to BSE infectivity," but the infectious theory was
still cast in the primary role because of the inability of Whatley to
show all four transformations.
Purdey
was not about to give up. He felt that there must be a co-factor that
he had missed. To find it he went on a tour of places in the world
where spongiform encepalopathies had existed in animals or humans for
some time, collecting samples of soil and feed. In these places, where
organophosphates had little or no use, he found extremely high
Manganese levels and low Copper, Selenium, Zinc and Iron. He did not
find this in geographically similar areas where no illness was found.
The causes of this mineral imbalance varied, including acid rain,
volcanic emissions, lead-free gasoline production, emissions from
steel, glass, ceramic, dye and munitions manufacturing and the
take-off zones of major airports.
BSE-like
diseases were found in Colorado among deer and elk in an area of the
front ranges where overpopulation often forced starving animals to
graze on pine needles. These showed very high levels of Manganese,
perhaps due to acid rain from upwind smelters. In Iceland, Purdey
found Scrapie associated with similar high Manganese/low Copper soil
conditions. In Slovakia the two clusters of CJD are close to
ferromanganese factories and glassworks (heavy users of Manganese).
These cases may well be related to the almost eradicated occupational
disease known as "Manganese Madness" which occurred among miners
exposed to poorly ventilated working conditions. Its symptoms and
brain pathology are similar to spongiform encephalopathies.
Purdey
was not just randomly testing for mineral abnormalities. Copper is a
constituent of the normal prion protein, and Manganese could be a
replacement when Copper is deficient, or when Manganese is present at
high levels, such as in many mineral supplements for cattle. It is at
this point that Organophosphates re-enter the theory. They can remove
copper from the body, leaving the door open for Manganese (or other
similar metals) to replace it in the prion protein. This results in a
non-functional conformation of the molecule, particularly when
Manganese is from the 2+ form to the oxidative 3+ and 4+ forms.
Recently, Purdey traveled to Groote Eylandt, an island north-east of
Australia where 25% of the world’s Manganese is currently produced.
About one in thirty people in the largely aboriginal Agurugu village,
where the fine mine dust regularly settles most heavily, have Groote
Syndrome, a progressive neurological disease. Researchers supported by
the mining company hypothesize a genetic defect introduced by
Portuguese sailors 300 years ago, even though this theory does not
explain why some white mine workers also have this syndrome, nor does
it explain the emergence of this syndrome since open pit mining began
in the 1960s.
Purdey’s theory was now multi-factorial. Organophosphates were a major
factor, but the copper/manganese imbalance could be exacerbated by
animal feeds or mineral supplements. Similar situations could occur
where the soil is low in the antioxidant metals and high in Manganese.
After
extending the theory, David Brown, a researcher at Cambridge
University performed experiments that incorporated high Manganese and
low Copper conditions and was able to reproduce all four protein
changes in vitro, thus providing full laboratory confirmation that
Purdey's theory is at least plausible.
At the
height of the Mad Cow frenzy, the British government invited Purdey to
make a detailed proposal for research funding. Predictably, after
sitting on the proposal for more than a year, they rejected it, and
then funded two of its reviewers for some of the studies suggested by
it. A cynic might conclude that they had asked for a grant proposal
solely to have Purdey reveal his arguments and thoughts in full
detail, so that they could then fund some ‘reliable’ researchers to
debunk them, without giving Purdey resources that might strengthen his
arguments.
Interest in Purdey’s ideas is still growing in a grass roots fashion,
although slowly, and usually beneath the radar of major media outlets.
Purdey has a small grant from the US Fats and Protein Research
Foundation, supervised by Dr. Larry Berger of the Animal Science Lab
in Urbana, Illinois. Purdey recently gave 14 lectures in Japan, some
Slovakian researchers are studying the influence of Manganese and
Copper on familial and sporadic cases of CJD. Some British
universities are also quietly investigating in this area.
Purdey
is attempting to obtain brain samples from Groote Eylandt to test for
manganese and copper levels, and has persuaded one local GP there to
see whether a chelating drug that removes Manganese will have
beneficial effects.
Purdey
is now investigating whether ultra-violet light is an additional
factor in the development of SE diseases, perhaps in concert with a
haze of terpines from the pine trees that often grow at these
elevations. He hypothesizes that the eyes could act as a trigger,
because of their concentration of nerves exposed to light.
Purdey
and other researchers have turned up many potential factors that could
stimulate the development of spongiform encephalopathies and chronic
wasting diseases. If some or all components of this theory prove to be
valid, the solutions to these devastating diseases could be incredibly
simple. It may also open new avenues of research into mental illness.
Supplementation of cattle feeds with minute amounts of copper and
regulation of the manganese levels could work near miracles, at
minimal cost. Chelation could be used to reduce the levels found in
people or animals suffering from these illnesses. Yet, it is likely
that governments and the scientific establishment will continue to
concentrate their efforts almost exclusively on infectious agents and
genetic defects, suppressing anybody brave enough to argue against
them on this or other health issues.
_______________
Mark
Purdey can be reached via his website:
http://www.markpurdey.com or by email to
MadCowPurdey@aol.com.
Further
Reading:
The
Inquiry into BSE and variant CJD in the United Kingdom:
http://www.bse.org.uk.2000
Purdey
M. Ecosystems supporting clusters of sporadic TSEs demonstrate
excesses of the radical-generating divalent cation manganese and
deficiencies of antioxidant cofactors Cu, Se, Fe, Zn. Medical
Hypotheses, 2000; 54(2), 278-306
Brown
DR et al. Consequences of Manganese replacement of Copper for prion
protein function and proteinase resistance. EMBO J, 2000 Mar 15;
19(6): 1180-6.
Purdey
M. The Purdey Environmental Home Page:
http://www.markpurdey.com
_______________
David Crowe writes on medical and telecommunications topics and is
a regular contributor to redflagsweekly.com. He has a degree in
biology and mathematics and has peer-reviewed papers published in the
areas of biosystematics and computer science. |