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
in Bethesda, Md., echoing the conventional view on mad cow disease and
vCJD, wrote in the April 7 edition of the British Medical Journal 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 Brown
believes that manganese may play an important role in a complex process
that eventually destroys the brain, both in cows and humans.
David 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 ground 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."
David 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.
