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Educating RIDA*
An underground scientific journey
into the origins of spongiform disease
by Mark Purdey
*ri da: (ICELANDIC) n. transmissible
spongiform disease; wasting disease of ruminant animals, such as cattle
and sheep
Since 1986, the infamous neurodegenerative syndrome known as Bovine
Spongiform Encephalopathy (BSE) has blighted the heartbeat of British
Agriculture. The disease has led to the annihilation of thousands of
cattle, whilst its human analogue, new-varient Creutzfeld Jakob Disease
(vCJD), has blighted the lives of a growing number of young people.
Moreover, the spongiform epidemic has created 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 terrible illness.
This story is an attempt to shine a ray of light over the whole debacle.
It charts my own eco-detective escapades and original field investigations,
which ran in tandem with the laboratory research of Cambridge University
biochemist, Dr. David Brown. These works have gone a long way towards
unearthing the truth underpinning the original cause of these grotesque
diseases.
Hard evidence has been amassed so far which indicates that vCJD and
BSE could both result from separate exposure of cattle and humans to
the same set of toxic environmental factors--excess manganese and oxidizing
agents--and not from the ingestion of beef by humans and animal by-products
by cows. If this hypothesis continues to accumulate corroborative evidence,
a radical upheaval of the status quo mindset can be expected.
Despite the fact that my theory has been substantiated both by field
and by laboratory findings, Dr. Brown's and my own 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 our grant proposals continues
to the present day, including one submission aimed at developing a feasible
cure for vCJD!
The Lone Voyager
My story begins in 1984 with the Ministry of Agriculture, Fisheries
and Food (MAFF) Warble Fly Order, which called for compulsory treatment
of UK cattle with toxic organophosphate insecticides. I fought the order
for my own pedigree Jersey cattle herd and won a precedent High Court
Judicial Review ruling against MAFF, debarring their enforced insecticide
treatment of my cows.
The insecticides applied to the backlines of UK cattle was called
Phosmet, a systemic acting chemical that, amongst a myriad of toxicological
effects, disturbs the crucial balance of metals in the brain. I was
therefore not surprised to witness BSE rearing its ugly head in UK cattle
in 1986. In my opinion, this was a direct legacy of the UK government's
warble fly mandate that exclusively enforced an annual dose rate that
was four times higher than the application rates employed in the few
other countries that used this type of insecticide.
(Phosmet, by the way, was produced by ICI Zeneca, which held the patent
on it until March 1996, the same month that BSE was announced in humans.
The patent was then sold to an unknown company in the Arizona desert
called Gowans.)
I was a working dairy farmer with first-hand experience of BSE erupting
in cattle that had been purchased into my organic farm. But I 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 percent conventional feeding stuff allowance decreed
in the organic standards.
The UK government was quick to blame the origins of BSE on the mysterious
"scrapie agent," a malformed protein or "prion" found in the brains
of all sheep who are suffering from the age-old neurodegenerative disease,
scrapie. The "experts" argued that this supposedly "infectious" agent
had jumped across from sheep into cows as a result of feeding cows with
meat and bone feed that had been contaminated with scrapie-affected
sheep brains. Relaxation of the rules governing the manufacture of MBM
in the early 1980s was supposed to have initiated the BSE epidemic.
Flaws in the Conventional Hypothesis
From the beginning the flaws in the Establishment's theory were evident:
- Thousands of tons of the incriminated UK MBM feed was exported
for cattle feed during the 1970s, 1980s and 1990s to areas that have
remained BSE-free to date, such as South Africa, Sweden, Eastern Europe,
Middle East, India and other Third World countries.
- Changes in the temperature and manufacturing techniques of the
MBM rendering process in the UK were blamed for permitting the survival
of the scrapie agent in dead sheeps' brains, enabling the "agent"
to jump across into cattle, thereby producing BSE. Yet in other scrapie-endemic
countries, such as USA and Scandinavia, the exact same continuous
flow system of rendering was adopted five years before the UK, yet
these countries remained BSE-free.
- Several US trials failed to invoke BSE in cattle after feeding
or injecting them with massive doses of scrapie-contaminated brain
tissue.
- More than forty thousand cows 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.
- There have been no cases of BSE in the other ruminants, such as
goats and sheep, susceptible to transmissible spongiform encephalopathy,
despite the customary inclusion of an MBM protein source in their
feeds.
- Four of the original five kudu antelope that developed BSE at the
London zoo had no possible access to MBM-containing feeds.
- The UK government's former experimental farm at Liscombe on Exmoor
was designed to raise suckler beef cattle on a pure grass-and-silage
system without any resort to feeding concentrated feeds at all. Yet
BSE struck down four animals on this holding.
- The UK's mechanically processed meat products and baby foods blamed
for causing vCJD in humans 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 has been practised
by the smaller butchers all over the UK for centuries without any
outbreak of vCJD.
Despite the myriad of epidemiological flaws and millions of dollars
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 has become gospel to the mainstream public
and professional mentality.
It is easy to see how such a reductionist mindset took hold: the media
loved the theory because they could drum up a viral holocaust-horror
scoop. The vegetarian lobby found themselves endowed with a powerful
propaganda weapon on their plate, whilst the scientific institutions
could carry on drawing generous funding for their hyperinfectious witch-hunt
without the embarrassment of having to account for years of barking
up the wrong tree. And the government could conveniently off-load 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 is the presence of a malformed protein--
known as the "prion"--in the nervous system of diseased mammals. But
none as yet has explained how and why this "prion" is originally formed
in the natural world.
I became interested in the possibility that the systemic OP warble
fly insecticides--which had to be poured along backline of the cow just
millimeters away from the prion protein-expressing cells in the spinal
cord--may trigger this malformation in some way, thereby serving as
the primary cause of the disease.
It is well recognized that OP insecticides exert their toxic effects
in mammals by deforming the molecular shape of various nerve proteins
to the extent that they cease to perform their proper function in the
brain. But none had ever considered that OPs could deform the prion
protein in this way.
After many abortive attempts to coerce the Establishment into running
the correct laboratory test, I eventually managed to raise funds from
well-wishers and personal loans to finance Dr. Stephen Whatley of the
Institute of Psychiatry in London to challenge brain cell cultures with
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. But these experiments did not
produce the key deformation of the prion protein that represents the
central hallmark of the transmissible spongiform encephalopathy (TSE)
diseased brain. I returned to square one, assuming that OPs in combination
with a further factor X could provide the final missing link.
The Cluster Buster
I grew exhausted by the vortex of the mad politico-medico-multinational
grand alliance that had successfully hijacked all UK scientific research
into TSEs. I embarked upon a refreshing global trek to analyze the unique
environments where traditional TSEs had erupted as high incidence clusters
for many years.
After tramping the world's most clear-cut TSE cluster zones in Colorado,
Iceland, Slovakia, Calabria and Sardinia, where an assortment of animals
and humans had developed TSE at exceptionally high rates, I discovered
a common factor - abnormally high levels of the metal manganese, and
rockbottom levels of copper, selenium and zinc in all of these food
chains. Manganese levels were normal in adjoining disease-free areas.
The Men from Manganese
A specific environmental source of manganese could be pinpointed in
each cluster zone tested, where each habitat occupied by the TSE-affected
species in question could be directly connected to the atmospheric fallout
of some naturally occurring or industrial source of combusted manganese
oxide, stemming from volcanic, acid rain; steel, glass, ceramic, dye
and munitions factories; lead-free petrol refineries; the takeoff airspace
beyond airports, and so forth.
My observations enabled me to construct a holistic hypothesis on the
aetiology of TSEs, work that lead to my connecting with the pioneering
laboratory studies of Dr. David Brown at Cambridge, a widely published
biochemist who had single-mindedly pursued his groundbreaking studies
on the elusive prion protein.
Dr. Brown demonstrated that in the normal healthy brain, the prion
protein bonds to copper and that this copper-protein can exert an antioxidant
function.
Brown's lab studies were complementary to my field studies, thereby
providing the other half of the necessary ground work upon which I devised
a hypothesis proposing that manganese could substitute itself at the
vacant copper site on the prion protein; the substitution occurring
in susceptible mammals who were entirely self sufficient upon high-manganese,
low-copper food chains.
I considered that this manganese substitution 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 necessary cell culture
experiments in which he introduced manganese into cells which manufacture
prion protein. Remarkably, this experiment produced the key prion protein
deformation which the earlier tests using OPs had failed to create.
Follow-up trials by Case Western University in Cleveland and a French
team of scientists provided further confirmation. Both groups ran postmortem
analyses of brain tissue taken from those who had died of conventional
CJD. These tests revealed the same pattern of high-manganese, low-copper
as identified in TSE food chains, a tenfold increase of manganese levels
and 50 percent 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 with high levels of silver, another transition metal,
instead of manganese. Much like manganese, silver will also readily
substitute at copper ligands on prion proteins. These environments were
centered around ski resorts, reservoirs, airport flight paths and coastal
districts where extensive aerial spraying of silver iodide "cloud seeding"
chemicals had been used for inducing rainfall, snowfall and cloud or
fog dispersion.
Further Daylight on TSEs
Another observation: each time my trek led me to a new TSE hotspot,
I found myself 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 me. Whenever I arrived at a fresh TSE location,
I was always reminded of that first glimpse of the chronic wasting countryside
of deer and elk in Colorado--the snow-peaked Rocky Mountains sawtoothing
the July skyline beyond the parched Denver Plain.
It was after arriving in a village in Calabria, on the southern tip
of Italy, that the relevance of this geographical connection to TSE
finally gelled. There had been 20 cases of CJD in this village since
1995. I noted that the village had been recently constructed out of
hideous bright white concrete sections--unusual for this area --and
all were couched within a sun-parched, glaring basin of bare white sandstone
terrain, producing all the prerequisites required for a most intensive
ultra violet (UV) hotspot location. The pain of the UV in my eyes immediately
connected me back to the high-UV / high ozone nature of high-altitude,
snow-covered, coniferous terrain--the common geographical thread interlinking
the Icelandic, Colorado and Slovak cluster ecosystems in my study--areas
also impacted by the oxidizing effects of the ozone gas generated by
the interaction of UV light with 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, eyelid or skin of the affected
mammal--external areas having to buttress front line exposure to sunlight.
Furthermore, the normal copper-bound form of prion protein is found
along the circadian pathways which conduct the electromagnetic energy
generated by ultraviolet light around the brain; that is, in the retina,
pineal gland, visual cortex, hypothalamus, pituitary and brain stem
(See illustrations).
Prion protein is expressed in other tissues of the body which are also
interconnected to the network that conducts electromagnetic energy,
for instance in the spleen, lymphatic system, glial cells and nerve-growth-factor-mediated
stem cells that proliferate during the growth and repair of neurons.
In this respect, the suggestion of an electro-conducting function
of the copper prion protein may turn out to give further scientific
substance to the existence of the electromagnetic meridians recognized
by Chinese medicine, where the healthy copper prion performs a regulatory
role in maintaining the electro-homeostasis along these meridians.
The hypothesis was falling into place: copper prions as the conductors
and manganese prions as the blockers of electromagnetic energy flow.
The fact that copper is used in wires that carry electric currents,
whereas manganese is used in batteries and light bulb filaments that
store electrical energy, helps explain the underlying cause of prion
diseases: healthy copper prions conduct the vital electro-energy of
sunlight along the circadian pathways that innervate deep into the brain--in
order to maintain the balanced cycles of sleep, sex and behavior whilst
aberrant manganese-contaminated prions blockade and store up that incoming
UV energy to an explosive flash point--to a level that detonates off
neuropathogenic cluster bombs of free radical chain reactions along
the circadian pathways.
With an overabundance of manganese prions and loss of copper prions,
the oxidative impact of UV energy received at the retina can no longer
be quenched. Consequently, the energy flow of UV piles up, finding itself
misappropriated into converting the accumulated store of innocuous manganese
2+ ( antioxidant ) into its lethal manganese 3+ or 4+ form (pro-oxidant).
So any accumulations of abnormal manganese prion protein in the retina
finds itself transformed from a safe to a lethal form.
In this respect eco-oxidants such as UV serve to unleash a kind of
"Jekyll and Hyde" effect in the manganese-contaminated, copper-depleted
mammal, which, in turn, kicks off a whole chain reaction of free radical
assault on the central nervous system--ultimately resulting in a neurodegenerative
meltdown that leads to spongiform disease.
The Cocktail of Oxidants and New Variant TSEs
This theory explains the genesis of the traditional strains of TSE.
But what about the causes of the much more aggressive modern day strains
of TSE (BSE and vCJD) surfacing in younger mammals? Perhaps these "rapid
attack'" new strain TSEs could result from our increased exposure to
the more potent oxidizing effects of a cocktail of man-made environmental
agents which can penetrate the central nervous system--contaminants
such as the systemic organophosphates (head lice shampoos, warblefly
pesticides), radar, ozone, increased UV (due to stratospheric ozone
depletion), microwave mobile phones, Concorde's supersonic waves, and
so forth, 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 homeostasis within the organism, where TSE-susceptible
mammals living in environments that are simultaneously challenged by
high intensities of manganese and oxidizing agents, and by low levels
of antioxidant metals (copper, selenium and zinc) which all combine
to create circumstances where the central nerves are severely hyper-oxidized,
thereby kicking off free radical chain reactions that are free to proliferate
in the absence of antioxidant defence.
The pattern of emergence of both traditional and new variant CJD clusters
in rural and coastal areas, as opposed to urban areas, substantiates
this oxidative origin idea well. Furthermore, the 80 percent predominance
of CJD cases erupting in rural and coastal areas helps to dispel the
myth that vCJD arises from ingestion of BSE-affected beef products,
as meat products are consumed equally by urban and rural populations.
Rural and coastal areas have become increasingly exposed to a toxic
cocktail of oxidizing agents, such as UV light, ozone and systemic crop
sprays; whereas town environments have ironically been spared. This
is largely due to the shield of smog that envelopes the majority of
urban airspaces and serves to scatter and absorb the incoming UV rays;
thereby preventing the UV - exhaust gas interaction that yields the
deadly consequences of ozone gas formation. It is perhaps no surprise
that the hyperoxidative environs of Staten Island and Long Island, which
plays host to an oxidative cocktail of Concorde takeoffs, radar, microwaves,
coastal UV and ozone, demonstrates the most intensive cluster of CJD
in the US.
Manganese Breaketh Man
The high-manganese connection to the epidemic of the new variant TSE
correlates as convincingly as the eco-oxidant connection. Over the last
two decades, increased amounts of the high concentration "manganese
oxide" additive have been introduced into the bovine, human, pet and
zoo animal food chains in Europe as mineral licks, tablets, fertilizer
and fungicide sprays, paints, and petrol additives. Another "trendy"
vector for manganese exposure is the increased consumption of soy, which
bioaccumulates excessive levels of this metal from the soil, whilst
containing low levels of copper.
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. Excess dietary manganese
poses a great risk to the immature mammal, since the homeostatic regulatory
mechanisms of the blood brain barrier are underdeveloped at this early
stage, thereby permitting an excessive uptake of manganese and other
metals into the brain. The dubious practise of adding soy as a protein
booster to these powders only serves to exacerbate the manganese toxicity
problem further!
Some would question how the toxic manganese-oxidant theory of TSE
origins can account for the well recognized "iatrogenic" forms of TSE,
where growth hormone treatment of humans (which utilizes pituitary tissue
as the inoculant) can lead to a form of CJD. The answer lies in the
fact that tissues, such as pituitary and retina that are considered
to transmit TSE in the lab most efficiently, are the exact same tissues
in which manganese concentrates 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
pro-oxidant 3+ form?
Future Pathways
Despite the apparent reluctance of establishment bodies to address
the works of David Brown and myself, we have both been independently
driven to take this theory to its final conclusive stages.
But funding has not been forthcoming, despite recommendations by the
UK's BSE Inquiry report, as well as MAFF's subsequent invitation asking
me 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, establishment recalcitrance has
blocked the development of a possible cure for new variant CJD, a study
that David Brown tried to launch last year.
In light of recent French and other European threats to sue the UK
for allegedly giving them BSE and vCJD, it is puzzling to witness the
continuation of the dismissive mindset that UK authorities display towards
any evidence that backs environmental involvement in TSEs; unbelievable,
in fact, after studying the recent work of Professor Bounias, from Avignon.
His study 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, I have continued to expand my field investigations by designing
a holistic environmental surveillance program involving metal and oxidant
analyses of relevant water, soil, vegetation, atmosphere, blood and
tissues that will be exercised in the variant CJD and BSE clusters that
have recently erupted across the UK and Europe, and now in Japan.
I have also been invited to study a cluster of mysterious progressive,
fatal neurodegenerative diseases, known as Bird's disease, that has
erupted amongst Aboriginal and Caucasian people living on Groote Eylandt,
a remote island ecosystem off the Northern Australian Coast. 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 conveniently scapegoated the
emergence of this syndrome--which manifests as a motor neurone disease
or a mystery dementia--onto a combination of Aboriginal genetics and
a rare virus that was introduced by a Portuguese miner who came to work
on the island three decades ago.
With permission from the local Aboriginal society, I hope to acquire
brain sections from those who have died of the TSE-like "dementia" strain
of this disease and see whether TSE-prion "tombstone" features can be
detected.
I have also managed to persuade a local GP in Darwin to treat some
of the early stage victims of Bird's disease with the manganese chelating
drug EDTA. Until now, victims of this grotesque disease have been kept
in total darkneww regarding the existence of a possible cure for a disease
that has always been considered fatal.
Sidebar Articles
Transmissible Spongiform Encephalopathies
Transmissible Spongiform Encephalopathies (TSEs) are a group of progressive
neurodegenerative diseases that emerge as three basic types: the inherited
familial forms, the traditional, long-standing sporadic forms, and the
new variant forms.
The inherited familial forms are strongly linked to a mutation on the
prion protein gene, although environmental factors are involved in triggering
the TSE. The profile of these TSEs is characterized by a slow degeneration
of the central nervous system, ultimately ending in dementia, motor
difficulties and death. Gerstmann-Straussler-Scheinker disease progresses
slowly over about five years; Fatal Familial Insomnia begins with bizarre
sleep and sexual disturbances and rapidly progresses to a fatal chronic
insomnia lasting just a few months.
The traditional forms of TSEs appear in older mammals and have a variety
of names depending on the species of animal: scrapie in sheep and goats,
chronic wasting disease in deer and elk, transmissible mink encephalopathy
in mink, and sporadic Creutzfeldt Jakob disease (CJD) in humans. These
sporadic forms of TSE exhibit a brain pathology that is characterised
by spongiform degeneration and loss of neurons in many regions of the
brain (such as the cortex), gliosis, shrunken basal ganglia and prion
rods (fibrils of aggregated proteins, mainly composed of misfolded prion
protein). Symptoms involve behavioural and cognitive disorders progressing
to visual, motor and sensory disorders, then ataxia, muscle wasting,
seizures, insanity and death.
The modern new variant forms appear as Bovine Spongiform Encephalopathy
(BSE) in young cows, cats, antelopes and new variant Creutzfeldt Jakob
disease (vCJD) in young humans. These new variant forms involve an accelerated,
more aggressive course of the disease involving a more widespread unique
neuropathology characterized by florid plaques (plaques surrounded by
spongiform holes) with more pronounced psychiatric disorders.
BSE in Britain - A Sad History
The first official reports of BSE outbreak were in 1986 from the southeast
of England, although many vets, farmers and slaughterers had suspected
a trickle of cases from the late 1970s onwards. The disease has been
an economic disaster for British farming interests as many cows were
slaughtered and British beef was banned from Europe. The disease rapidly
developed into a massive bell shaped epidemic which peaked in 1992 at
36,680 cases in the year and dwindled back to 1000 cases a year where
the incidence rate stands at today. BSE has taken nearly 200,000 confirmed
cases to date. The disease was largely concentrated in the South of
England during early days; it erupted in some remote Scottish districts
in later years due to the importation of the warble fly in cows being
brought from Europe and who were then treated with organophosphates.
Manganese In Human Nutrition
Manganese in small amounts plays an important role in human nutrition.
It forms an essential cofactor of numerous enzymes and is necessary
for the utilization and balanced metabolism of many other nutrients.
Manganese is a catalyst in the synthesis of fatty acids and cholesterol
and is essential for the production of sex and thyroid hormones. Because
manganese plays a role in the mitochondial "power stations" of the nerve
neurones, deficiency can result in symptoms that are similar to those
of overload--lack of coordination, irritability, psychological difficulties
and even paralysis, convulsions, blindness and hearing loss.
Whole grains, egg yolks, nuts, seeds and green vegetables provide
manganese if it is present in the soil. Manganese is poorly absorbed
from food but readily absorbed into the brain via the inhalatory-nasal-olfactory
route. Thus toxicity is much more likely from environmental atmospheric
sources than from food, although diets high in manganese-containing
foods, such as soy and tea, can exacerbate the condition of manganese
overload, especially when fed in large amounts to infants or growing
animals.
Meat and Bone Meal (MBM) Feeding Vs. Soy
Protein sources have always been in keen demand for feed concentrate
ingredients in confinement dairies and feed lot operations in the developed
world, where rations demand a 14-18 percent protein concentration. Waste
animal protein derived from the rendered down remains of butchered livestock
(alongside various plant protein sources) has been used in animal feeding
stuffs since the 1920s--surprisingly, with no known ill effects! The
BSE outbreak was blamed on changes in MBM manufacturing methods (such
as use of lower temperatures and cessation of solvent extraction) and
resulted in the substitution of large amounts of processed soy meal,
as well as some fish proteins, for cattle feed. In fact, the BSE epidemic
has been a boon for soybean growers and manufacturers. Soy has been
used for many years as a principle ration for chickens and salmon (both
meats allowed in the politically correct modern lowfat diet) but was
not normally given in large amounts to ruminant animals because of the
damage it inflicted on their livers. Now that MBM is banned in the US
and Europe, the multinational-controlled GM soy industry has a large
pool of new customers, not only among confinement dairies and large
feedlot operations, but also among thousands of new vegetarians, anxious
to avoid "mad cow" disease.
Kuru
Similar to CJD, kuru is a progressive neurologic disorder that occurs
primarily in the Fore natives who inhabit a tiny pocket of the New Guinea
highlands. Symptoms are much like vCJD and include an exaggerated startle
response and emotional instability, with pathologic bursts of laughter.
Advanced states are characterized by dementia. In the terminal state,
the patient is generally totally placid, mute and unresponsive.
Until the early 1960s, the disease was prevalent, especially in women
and children, but in recent years the incidence has declined. This was
said to be due to the abandonment of ritual cannibalistic practices
in which natives ate the flesh of the dead, a theory that fit in very
well with the dogma that the bovine version was caused by consumption
of infected meat and bone meal. But the entire native population across
New Guinea were traditionally involved in cannibalism, so why Kuru in
just one tiny region? A more likely explanation is the massive eruption
of a local volcano in 1911 which showered the foodchain of the Fore
region in a black manganese oxide ash--the decline in kuru paralleling
the importation of more foodstuffs from the outside world. Both the
early stage unmotivated laughter with psychosis, and the placid, unresponsive
characteristics of advanced kuru are similar to the symptom profile
of manganese poisoning.
Addendum (Letter to the Weston A. Price Foundation from Mark Purdey,
which appeared in the Summer 2002
edition of Wise Traditions):
Mad Deer
It has been such an impressionable experience here in Australia studying
a local variant of wasting disease. Whilst the neurological disease
problem lies in a manganese induced mutation, via a combination of genetical
susceptibility and excessive manganese, plus low magnesium, there are
some major, major inadequacies with the modern day Aboriginal diet.
It's the worst I have seen, in fact: Coca-Cola, white bread, sugar,
sugar, and sugar! I kept on remembering Weston A Price's reports on
the Aboriginal people with their beautiful teeth. Some kids in their
twenties have lost all their teeth these days.
I did find out a very important piece of information which explains
the cause of chronic wasting disease in deer. The hunters in Wisconsin
and Colorado have been putting down a dual purpose mineral block designed
to addict the deer to the hunters' shooting territory as well as supplying
manganese for making the antlers grow big. They have been using this
stuff exactly where chronic wasting disease has burst out.
Mark Purdey
Somerset, UK
About the Author
 As
an organic dairy farmer, the late Mark Purdey of Somerset UK,
resisted the order to spray his cattle with organophosphates for warble fly
and went to court for a judicial review; he won and was exempted from using
the spray. No cows born in his herd developed BSE (mad cow disease). Mark contributed
numerous articles on the subject of BSE to scientific journals based on his
"ecodetective" investigations of select regions around the world where
clusters of various brain diseases have emerged. His technique of geochemical
analyses of the levels of metals, radioactivity, magnetic status, etc., within
the ecosystems where clusters of Alzheimer's, Parkinson's, motor neuron, multiple
sclerosis and Creutzfeldt-Jacob (mad cow) diseases have emerged, enabled him
to isolate various common toxic denominators which could represent the causal
agents. Mark's published data and novel hypotheses indicate that the specific
metal microcrystal pollutants (manganese, barium, strontium, etc.) that he observed
at high levels in the cluster environments, will "seed" an aberrant
growth of rogue metal-protein crystals within brain tissues; thereby initiating
the pathogenesis of these diseases. He advised HRH Prince of Wales and UK government
ministers, and delivered numerous lectures to universities—Harvard, Cambridge,
Tokyo, Torino—across the world.
Also of Interest
This article appeared in Wise Traditions
in Food, Farming and the Healing Arts,
the quarterly magazine of the Weston A. Price Foundation, Spring 2002.
Click
here to become a member of the Foundation and receive our quarterly
journal, full of informative articles as well as sources of healthy food.
Copyright Notice: The material
on this site is copyrighted by the Weston A. Price Foundation. Please contact
the Foundation for permission if you wish to use the material for any purpose.
Disclaimer: The information published herein is not intended
to be used as a substitute for appropriate care by a qualified health practitioner.
The Weston A. Price Foundation
PMB 106-380, 4200 Wisconsin Ave., NW, Washington DC 20016
Phone: (202) 363-4394 | Fax: (202) 363-4396 | Web: www.westonaprice.org
General Information/Membership/Brochures:
Local Chapters and Chapter Leaders:
Website:
This page was posted on 30 JUN 2002.
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