Mad Cow update:
Could the Environment
Trigger Mad Cow Disease?
Controversial Research Says Metals —
Not Infectious Beef — May Be Involved
Commentary
By Nicholas Regush
May 29 — What if it turns out that the human form of
mad cow disease is triggered by environmental factors
— and not by infectious beef products — as some
ongoing British research at Cambridge University
suggests?
STORY HIGHLIGHTS
Conventional View Controversial View A Metal Can
Change Brain Chemistry Pesticides May Play Role, Too
More Research Necessary
What if much of the science to date, focusing on
contaminated meat, has been overly simplistic or even
dead wrong?
The immediate implication would be that we would have
to rethink everything already done to fight the
disease, both in Britain where it began, in Europe,
where it has spread, and in other nations, including
the United States, where concerns are mounting about
its potential to be unleashed.
Last week, in order to prevent the disease from
contaminating the blood supply, the American Red
Cross, in accepting the view that infectious beef is
to blame, barred donations from anyone who
consecutively spent three months in Britain and six
months in Europe since 1980.
Presumably, anyone in those countries for that long a
period would have had the opportunity to contract an
infection from eating contaminated beef and then
possibly pass it on by donating blood.
But, of course, this prevention strategy presumed the
prevailing scientific perspective on mad cow disease
and its human form, variant Creutzfeldt-Jacob disease
or vCJD, is correct.
Conventional View: Consumed Infectious Agent
The viewpoint held by most scientists is that an
infectious agent likely moved from sheep to cows and
gained enough strength in its cross-species jump to
ravage the nervous system and cause the bovine brain
to appear spongy and rife with holes like Swiss
cheese. This brain-destroying "mad cow" infection was
further transmitted, according to this interpretation,
via the rendering of carcasses, to meat and bone meal
in feed. That set off the epidemic in British cows in
1986.
The human form of the disease began to turn up in
Britain in 1995 when, according to the conventional
wisdom, the infectious agent in cows, thought to have
been passed on to humans by contaminated cooked meat
products, had sufficient time to incubate and become
destructive to the nervous system.
So far, about 100 people have developed vCJD and died,
the majority of them in Britain. Mind and body are
usually destroyed within a year.
Paul Brown, a research scientist at the National
Institutes of Health (NIH) in Bethesda, Md., echoing
the conventional view on mad cow disease and vCJD,
wrote in the April 7 edition of the British Medical
Journal (BMJ) that it is "uncontestable" that the
disease in cows is the cause of vCJD.
But not according to David Brown, a biochemist at
Cambridge University, who counters that "there is no
conclusive proof that [mad cow disease] caused vCJD."
Next week at a scientific conference in Quebec City,
he'll discuss some of his most recent research,
pointing to a possible environmental explanation of
both mad cow disease and vCJD.
Controversial View: Environmental Exposure
That conference is all about manganese, a heavy metal,
that is essential to life and is part of the daily
diet — for example, wheat, rice and tea provide the
metal — but numerous studies show that environmental
overexposure to it can be dangerous to the nervous
system.
Manganese can affect humans via air, water and soil.
For example, workers who have been exposed to high
industrial doses of manganese have suffered tremors
and muscular rigidity, hallucinations, and involuntary
laughing and crying. Biochemical analysis of central
nervous system tissue in humans poisoned by manganese
shows that the metal can cause brain cells to die.
On the basis of his published laboratory research,
Cambridge's David Brown believes that manganese may
play an important role in a complex process that
eventually destroys the brain, both in cows and
humans.
Brown agrees with the conventional view that the key
agent in the disease is a protein called a "prion."
These prions are thought to keep nerve cells stable.
The conventional view holds that prions can somehow
become malformed and that's when they become
infectious and capable of damaging the brain.
The malformed prion, then, according to the
conventional view, is the infectious and transmissible
agent in mad cow disease and vCJD. The infection is
neither a virus, nor a bacterium.
A Metal Can Change Brain Chemistry
Brown parts company here with the conventional view,
altogether dismissing the notion of an "infectious"
prion. He told me: "I have [published] evidence from
my cell culture experiments that shows manganese can
change the prion into its abnormal [and dangerous]
form." This is especially the case when the supply of
copper to the cell is low.
If David Brown's research is on a correct path, then
scientific and public concerns about infection from
beef could eventually be dwarfed by concerns about
toxic effects in the environment that cause copper
levels to decrease and manganese levels to rise.
Because Brown's research shows that he can change the
prion from its normal to abnormal state by
manipulating the only two metals that bind to it,
copper and manganese, without the need for any
infectious material, he believes the reigning theory
about mad cow disease and vCJD is at best incomplete,
and quite likely incorrect.
So, he sees it as plausible that what is seen in the
test tube may also occur in humans who are
environmentally exposed to excess amounts of
manganese. (The metal's ancient Greek name is
manganin, which means the occult, voodoo or black
magic.)
In fact, Brown's research has given a boost to the
controversial theories of Mark Purdey, a farmer turned
amateur scientist who has been challenging the
conventional view of mad cow disease and vCJD from the
start.
He has provided detailed reports to the British
government's hearings on mad cow disease and has
published several peer-reviewed scientific papers on
the subject, including data on how manganese in the
environment may play a role in both mad cow disease
and vCJD.
Purdey never bought into the conventional wisdom. "It
never made any sense to me," he said in an interview
from his farm in Taunton, England.
Pesticides May Play Role, Too
His battle goes back to 1984 when farmers in many
locales were ordered by the government to use an
organophosphate pesticide (Phosmet) to fight off the
warble fly, a parasite that lays eggs under the skin
of cattle. Purdey, who operates an organic farm,
refused to do so, went to court and won.
This pesticide, a constituent of nerve gas, was
applied on the back of the cow along its spinal
column.
When mad cow disease erupted, Purdey noticed that the
disease occurred on farms where the pesticide was used
and not on those which, like his, it wasn't. He added:
"Also, no home-reared cows on organic farms have
developed [mad cow disease].
Purdey then focused his attention on geographic areas
where there had been reported clusters of mad cow
disease, similar illnesses and vCJD. "I discovered [in
sampling soil, water and vegetation] that the common
factor in the environment is manganese," he explained.
"In some case, huge amounts of it. Also, the amounts
of copper in these areas was low."
He presented his findings in his 28-page scientific
paper published last year in the journal, Medical
Hypothesis.
For example, in Iceland, he found high levels of
manganese deposits in valleys where a sheep disease,
scrapie, similar to mad cow disease flourished.
Valleys with normal manganese levels were
scrapie-free.
In Colorado, he found deer herds with high incidence
of a mad cow-like wasting disease were eating pine
needles loaded with manganese. "I brought the pine
needles home and had them tested and the manganese was
excessively high."
Closer to home, Purdey has also investigated several
cases of vCJD in the area of the village of
Queniborough and discovered that soil and water
samples showed high to very high levels of manganese.
In the '80s and '90s a dye-works plant operated in
Queniborough. Manganese is used in dyes, he said,
adding that villagers remembered days when a cloud of
yellow dust would settle in the area.
All his digging around has led to a highly detailed
theory for mad cow disease: In short:
The high doses of organophosphates that were
poured on the cows' spines and poisoned the bodies
decreased the amount of copper in cells.
The feed given to animals in the '80s contained
high amounts of manganese, some of it derived from
chicken manure of chickens fed high doses of manganese
to strengthen egg shells. Supplemental powders and
mineral licks with manganese were sometimes added to
feed troughs.
The depletion of copper and the high manganese
changes normal prions to abnormal, thus setting the
stage for disease.
Purdey believes vCJD is also likely triggered by
similar environmental factors.
But NIH's Paul Brown told me that this alternative
theory is among those he views as "nonsense,"
referring me to his BMJ paper of April 7.
In it, he states that the theory that organophosphates
are involved in mad cow disease fails to account for
the evidence that the disease can be experimentally
transmitted.
Purdey counters that the disease is not transmitted
experimentally when processed beef products are used.
Only when tissue directly from cows is grinded up and
mixed. "Humans and cattle obviously do not eat this
concentrated so-called "bovine homogenate," he
explained. "This is not the correct way to do
science."
When the homogenate is used, theorizes Purdey, its
toxicity, due to changes in its arrangement of metals,
may lead to a change in prions from their normal to an
abnormal state.
The NIH's Brown, also writing in BMJ, raises the
question of why Japan has been mad-cow free since it
uses organophosphates extensively.
Purdey's response is that Britain's use of Phosmet,
unlike elsewhere, was four times the maximum dose and
that it was an oil-based application that entered the
cows' blood stream. "You can't just simply throw
around the idea that everyone uses organophosphates
the same way."
More Research Necessary
So where do we stand on this issue? Obviously the
mainstream infectious model of what mad cow disease is
all about holds sway and is likely to continue to do
so. Unless, of course, more research funding is
granted to nay-sayers like Purdey and Cambridge's
David Brown that makes for compelling science and
headlines.
The British Government has paid some lip service to
Purdey's ideas — they have been discussed in the House
of Commons — and has promised him some research
funding. But so far, no dice.
David Brown of Cambridge, while cautious about his and
Purdey's challenge to conventional thinking on mad cow
disease and vCJD, said that "science should be open to
these possibilities, particularly since there is still
a lot of mystery surrounding these outbreaks."
Brown also believes that ignoring the possibility that
environmental factors trigger both animal and human
diseases could prevent action from being taken to
clean up toxic effects that may be at the root of the
problem. "We obviously need much broader research in
this entire area," he said.
This is a battle that will not likely go away. And it
shouldn't go away until more research is done to
examine the claims — on both sides.
DAK |
