October 2001, 34-year-old Washington State native Peter
Putnam started losing his mind. One month he was delivering a keynote
business address, the next he couldn't form a complete sentence. Once
athletic, soon he couldn't walk. Then he couldn't eat. After a brain
biopsy showed it was Creutzfeldt-Jakob disease, his doctor could no longer
offer any hope. "Just take him home and love him," the doctor counseled
his family.[1,2,3] Peter's tragic death, October 2002, may have been
caused by Mad Cow disease.
Seven years earlier and 5000 miles away, Stephen
Churchill was the first in England to die. His first symptoms of
depression and dizziness gave way to a living nightmare of terrifying
hallucinations; he was dead in 12 months at age 19. Next was Peter
Hall, 20, who showed the first signs of depression around Christmas, 1994.
By the next Christmas, he couldn't walk, talk, or do anything for
himself. Then it was Anna's turn, then Michelle's. Michelle Bowen, age
29, died in a coma three weeks after giving birth to her son via emergency
cesarean section. Then it was Alison's turn. These were the first five
named victims of Britain's Mad Cow epidemic.
They died from what the British Secretary of
Health called the worst form of death imaginable, Creutzfeldt-Jakob
disease, a relentlessly progressive and invariably fatal human
dementia. The announcement of their deaths, released on March 20, 1996
(ironically, Meatout Day), reversed the British government's decade-old
stance that British beef was safe to eat. It is now considered an
"incontestable fact" that these human deaths in Britain were caused by
Bovine Spongiform Encephalopathy (BSE), or Mad Cow disease. Bovine
means "cow or cattle," spongiform means "sponge-like," and encephalopathy
means "brain disease." Mad Cow disease is caused by unconventional
pathogens called prions--literally infectious proteins--which, because of
their unique structure, are practically invulnerable, surviving even
incineration at temperatures hot enough to melt lead. The leading
theory as to how cows got Mad Cow disease in the first place is by eating
diseased sheep infected with a sheep spongiform encephalopathy called
In humans, prions can cause Creutzfeldt-Jakob disease (CJD),
a human spongiform encephalopathy whose clinical picture can involve
weekly deterioration into blindness and epilepsy as one's brain becomes
riddled with tiny holes.
We've known about Creutzfeldt-Jakob disease for decades,
since well before the first mad cow was discovered in 1985. Some cases of
CJD seemed to run in families; other cases seemed to just arise
spontaneously in about one in a million people every year, and were hence
dubbed "sporadic." The new form of CJD caused by eating beef from cows
infected with Mad Cow disease, though, seemed to differ from the classic
The CJD caused by infected meat has tended to strike
younger people, has produced more psychotic symptoms, and has often
dragged on for a year or more. The most defining characteristic, though,
was found when their brains were sampled. The brain pathology was vividly
reminiscent of Kuru, a disease once found in a New Guinea tribe of
cannibals who ate the brains of their dead. Scientists called this new
form of the disease "variant" CJD.
Other than Charlene, a 24 year old woman now so
tragically dying in Florida, who was probably infected in Britain, there
have been no reported cases of variant CJD in the U.S. Hundreds of
confirmed cases of the sporadic form of Creutzfeldt-Jakob disease,
however, arise in the United States every year, but the beef industry
is quick to point out these are cases of sporadic CJD, not the new variant
known to be caused by Mad Cow disease. Of course, no one knows what
causes sporadic CJD. New research, discussed below, suggests that not
hundreds but thousands of Americans die of sporadic CJD every year, and
that some of these CJD deaths may be caused by eating infected meat after
Although the fact that Mad Cow disease causes variant
CJD had already been strongly established, researchers at the University
College of London nevertheless created transgenic mice complete with
"humanized" brains genetically engineered with human genes to try to prove
the link once and for all. When the researchers injected one strain of
the "humanized" mice with infected cow brains, they came
down with the same brain damage seen in human variant CJD, as expected.
But when they tried this in a different strain of transgenic "humanized"
mice, those mice got sick too, but most got sick from what looked exactly
like sporadic CJD! The Mad Cow prions caused a disease that had a
molecular signature indistinguishable from sporadic CJD. To the extent
that animal experiments can simulate human results, their shocking
conclusion was that eating infected meat might be responsible for some
cases of sporadic CJD in addition to the expected variant CJD. The
researchers concluded that "it is therefore possible that some patients
with [what looks like]... sporadic CJD may have a disease arising from BSE
exposure." Laura Manuelidis, section chief of surgery in the
neuropathology department at Yale University comments, "Now people are
beginning to realize that because something looks like sporadic CJD they
can't necessarily conclude that it's not linked to [Mad Cow
This is not the first time meat was linked to sporadic
CJD. In 2001, a team of French researchers found, to their complete
surprise, a strain of scrapie--"mad sheep" disease--that caused the same
brain damage in mice as sporadic CJD. "This means we cannot rule out
that at least some sporadic CJD may be caused by some strains of scrapie,"
says team member Jean-Philippe Deslys of the French Atomic Energy
Commission's medical research laboratory. Population studies had
failed to show a link between CJD and lamb chops, but this French research
provided an explanation why. There seem to be six types of sporadic CJD
and there are more than 20 strains of scrapie. If only some sheep strains
affect only some people, studies of entire populations may not clearly
show the relationship. Monkeys fed infected sheep brains certainly come
down with the disease. Hundreds of "mad sheep" were found in the U.S.
in 2003. Scrapie remains such a problem in the United States that the
USDA has issued a scrapie "declaration of emergency." Maybe some cases
of sporadic CJD in the U.S. are caused by sheep meat as well.
Pork is also a potential source of infection. Cattle
remains are still boiled down and legally fed to pigs (as well as
chickens) in this country. The FDA allows this exemption because no
"naturally occurring" porcine (pig) spongiform encephalopathy has ever
been found. But American farmers typically kill pigs at just five months
of age, long before the disease is expected to show symptoms. And, because
pigs are packed so tightly together, it would be difficult to spot
neurological conditions like spongiform encephalopathies, whose most
obvious symptoms are movement and gait disturbances. We do know, however,
that pigs are susceptible to the disease--laboratory experiments show that
pigs can indeed be infected by Mad Cow brains--and hundreds of
thousands of downer pigs, too sick or crippled by injury to even walk,
arrive at U.S. slaughterhouses every year.
A number of epidemiological studies have suggested a
link between pork consumption and sporadic CJD. Analyzing peoples' diet
histories, the development of CJD was associated with eating roast pork,
ham, hot dogs, pork chops, smoked pork, and scrapple (a kind of pork
pudding made from various hog carcass scraps). The researchers concluded,
"The present study indicated that consumption of pork as well as its
processed products (e.g., ham, scrapple) may be considered as risk factors
in the development of Creutzfeldt-Jakob disease." Compared to people that
didn't eat ham, for example, those who included ham in their diet seemed
ten times more likely to develop CJD. In fact, the USDA may have
actually recorded an outbreak of "mad pig" disease in New York 25 years
ago, but still refuses to reopen the investigation despite petitions from
the Consumer's Union (the publishers of Consumer Reports magazine).
Sporadic CJD has also been associated with weekly beef
consumption, as well as the consumption of roast lamb, veal,
venison, brains in general, and, in North America, seafood.[32,33] The
development of CJD has also, surprisingly, been significantly linked to
exposure to animal products in fertilizer, sport fishing and deer
hunting in the U.S., and frequent exposure to leather products.
We do not know at this time whether chicken meat poses a
risk. There was a preliminary report of ostriches allegedly fed risky feed
in German zoos who seemed to come down with a spongiform
encephalopathy. Even if chickens and turkeys themselves are not
susceptible, though, they may become so-called "silent carriers" of Mad
Cow prions and pass them on to human consumers. Dateline NBC quoted D.
Carleton Gajdusek, the first to be awarded a Nobel Prize in
Medicine for his work on prion diseases, as saying,
"it's got to be in the pigs as well as the cattle. It's got to be passing
through the chickens." Dr. Paul Brown, medical director for the US
Public Health Service, believes that pigs and poultry could indeed be
harboring Mad Cow disease and passing it on to humans, adding that pigs
are especially sensitive to the disease. "It's speculation," he says, "but
I am perfectly serious."
The recent exclusion of most cow brains, eyes, spinal
cords, and intestines from the human food supply may make beef safer, but
where are those tissues going? These potentially infectious tissues
continue to go into animal feed for chickens, other poultry, pigs, and
pets (as well as being rendered into products like tallow for use in
cosmetics, the safety of which is currently under review). Until
the federal government stops the feeding of slaughterhouse waste, manure,
and blood to all farm animals, the safety of meat in America cannot be
The hundreds of American families stricken by sporadic
CJD every year have been told that it just occurs by random chance.
Professor Collinge, the head of the University College of London lab,
noted "When you counsel those who have the classical sporadic disease, you
tell them that it arises spontaneously out of the blue. I guess we can no
longer say that."
"We are not saying that all or even most cases of
sporadic CJD are as a result of BSE exposure," Professor Collinge
continued, "but some more recent cases may be--the incidence of sporadic
CJD has shown an upward trend in the UK over the last decade... serious
consideration should be given to a proportion of this rise being BSE-related.
Switzerland, which has had a substantial BSE epidemic,
has noted a sharp recent increase in sporadic CJD." In the Nineties,
Switzerland had the highest rate of Mad Cow disease in continental Europe,
and their rate of sporadic CJD doubled.
We don't know exactly what's happening to the rate of
CJD in this country, in part because CJD is not an officially notifiable
illness. Currently only a few states have such a requirement.
Because the Centers for Disease Control (CDC) does not actively monitor
the disease on a national level, a rise similar to the one in Europe
could be missed. In spite of this, a number of U.S. CJD clusters have
already been found. In the largest known U.S. outbreak of sporadic cases
to date, five times the expected rate was found to be associated with
cheese consumption in Pennsylvania's Lehigh Valley. A striking
increase in CJD over expected levels was also reported in Florida and
New York (Nassau County) with anecdotal reports of clusters of deaths
in Oregon and New Jersey.
Perhaps particularly worrisome is the seeming increase
in CJD deaths among young people in this country. In the 18 years between
1979 and 1996, only a single case of sporadic CJD was found in someone
under 30. Whereas between 1997 and 2001, five people under 30 died of
sporadic CJD. So five young Americans dying in five years, as opposed to
one young case in the previous 18 years. The true prevalence of CJD among
any age group in this country remains a mystery, though, in part because
it is so commonly misdiagnosed.
The most frequent misdiagnosis of CJD among the elderly
is Alzheimer's disease. Neither CJD nor Alzheimer's can be
conclusively diagnosed without a brain biopsy, and the symptoms and
pathology of both diseases overlap. There can be spongy changes in
Alzheimer's, for example, and senile Alzheimer's plaques in CJD.
Stanley Prusiner, the scientist who won the Nobel Prize for his discovery
of prions, speculates that Alzheimer's may even turn out to be a prion
disease as well. In younger victims, CJD is more often misdiagnosed as
multiple sclerosis or as a severe viral infection.
Over the last 20 years the rates of Alzheimer's disease
in the United States have skyrocketed. According to the CDC,
Alzheimer's Disease is now the eighth leading cause of death in the United
States, afflicting an estimated 4 million Americans. Twenty
percent or more of people clinically diagnosed with Alzheimer's disease,
though, are found at autopsy not to have had Alzheimer's at all. A
number of autopsy studies have shown that a few percent of Alzheimer's
deaths may in fact be CJD. Given the new research showing that infected
beef may be responsible for some sporadic CJD, thousands of Americans may
already be dying because of Mad Cow disease every year.
Nobel Laureate Gajdusek, for example, estimates that 1%
of people showing up in Alzheimer clinics actually have CJD. At Yale,
out of a series of 46 patients clinically diagnosed with Alzheimer's, six
were proven to have CJD at autopsy. In another study of brain
biopsies, out of a dozen patients diagnosed with Alzheimer's according to
established criteria, three of them were actually dying from CJD. An
informal survey of neuropathologists registered a suspicion that CJD
accounts for 2-12% of all dementias in general. Two autopsy studies
showed a CJD rate among dementia deaths of about 3%.[69,70] A third study,
at the University of Pennsylvania, showed that 5% of patients diagnosed
with dementia had CJD. Although only a few hundred cases of sporadic
CJD are officially reported in the U.S. annually, hundreds of
thousands of Americans die with dementia every year. Thousands of
these deaths may actually be from CJD caused by eating infected meat.
The incubation period for human spongiform
encephalopathies such as CJD can be decades. This means it can be
years between eating infected meat and getting diagnosed with the death
sentence of CJD. Although only about 150 people have so far been diagnosed
with variant CJD worldwide, it will be many years before the final death
toll is known. In the United States, an unknown number of animals are
infected with Mad Cow disease, causing an unknown number of human deaths
from CJD. The U.S. should immediately begin testing all cows destined for
human consumption, as is done in Japan, should stop feeding slaughterhouse
waste to all farm animals (see
and should immediately enact an active national surveillance program for
Five years ago this week, the Center for Food Safety,
the Humane Farming Association, the Center for Media & Democracy, and ten
families of CJD victims petitioned the FDA and the CDC to immediately
enact a national CJD monitoring system, including the mandatory reporting
of CJD in all 50 states. The petition was denied.
The CDC argued that their passive surveillance system
tracking death certificate diagnoses was adequate. Their analysis of death
certificates in three states and two cities, for example, showed an
overall stable and typical one in a million CJD incidence rate from 1979
to 1993. But CJD is so often misdiagnosed, and autopsies are so
infrequently done, that this system may not provide an accurate
In 1997, the CDC set up the National Prion Disease
Pathology Surveillance Center at Case Western Reserve University to
analyze brain tissue from CJD victims in the U.S. in hopes of tracking any
new developments. In Europe, surveillance centers have been seeing most,
if not all, cases of CJD. The U.S. center sees less than half. "I'm very
unhappy with the numbers," laments Pierluigi Gambetti , the director of
the Center. "The British and Germans politely smile when they see we
examine 30% or 40% of the cases," he says. "They know unless you examine
80% or more, you are not in touch." "The chance of losing an important
case is high."
One problem is that many doctors don't even know the
Center exists. And neither the CDC nor the Center are evidently authorized
to reach out to them directly to bolster surveillance efforts, because
it's currently up to each state individually to determine how--or even
whether--they will track the disease. In Europe, in contrast, the national
centers work directly with each affected family and their physicians.
In the U.S., most CJD cases--even the confirmed ones--seem to just fall
through the cracks. In fact, based on the autopsy studies at Yale and
elsewhere, it seems most CJD cases in the U.S. aren't even picked up in
the first place.
Autopsy rates have dropped in the U.S. from 50% in the
Sixties to less than 10% at present. Although one reason autopsies are
rarely performed on atypical dementia cases is that medical professionals
are afraid of catching the disease, the primary reason for the decline
in autopsy rates in general appears to be financial. There is currently no
direct reimbursement to doctors or hospitals for doing autopsies, which
often forces the family to absorb the cost of transporting the body to an
autopsy center and having the brain samples taken, a tab that can run
upwards of $1500.
Another problem is that the National Prion Disease
Pathology Surveillance Center itself remains underfunded. Paul Brown,
medical director for the National Institutes of Health, has described the
Center's budget as "pitiful," complaining that "there isn't any budget for
CJD surveillance." To adequately survey America's 290 million
residents, "you need a lot of money." UK CJD expert Robert Will explains,
"There was a CJD meeting of families in America in which... [the CDC] got
attacked fairly vigorously because there wasn't proper surveillance. You
could only do proper surveillance if you have adequate resources." "I
compare this to the early days of AIDS," says protein chemist Shu Chen,
who directs the Center's lab, "when no one wanted to deal with the
Andrew Kimbrell, the director of the Center for Food
Safety, a D.C.-based public interest group, writes, "Given what we know
now, it is unconscionable that the CDC is not strictly monitoring these
diseases." Given the presence of Mad Cow disease in the U.S., we need
to immediately enact uniform active CJD surveillance on a national level,
provide adequate funding not only for autopsies but also for the shipment
of bodies, and require mandatory reporting of the disease in all 50
states. In Britain, even feline spongiform encephalopathy, the cat version
of Mad Cow disease, is an officially notifiable illness. "No one has
looked for CJD systematically in the U.S.," notes NIH medical director
Paul Brown. "Ever."
The animal agriculture industries continue to risk
public safety, and the government seems to protect the industries' narrow
business interests more than it protects its own citizens. Internal USDA
documents retrieved through the Freedom of Information Act show that our
government did indeed consider a number of precautionary measures as far
back as 1991 to protect the American public from Mad Cow disease.
According to one such document, however, the USDA explained that the
"disadvantage" of these measures was that "the cost to the livestock and
rendering industries would be substantial."
Plant sources of protein for farm animals can cost up to
30% more than cattle remains. The Cattlemen's Association admitted a
decade ago that animal agribusiness could indeed find economically
feasible alternatives to feeding slaughterhouse waste to other animals,
but that the they did not want to set a precedent of being ruled by
Is it a coincidence that USDA Secretary Veneman chose
Dale Moore, former chief lobbyist for the National Cattlemen's Beef
Association, as her chief of staff? Or Alison Harrison, former
director of public relations for the Cattlemen's Association, as her
official spokeswoman? Or that one of the new Mad Cow committee
appointees is William Hueston, who was paid by the beef industry to
testify against Oprah Winfrey in hopes of convicting her of beef
"disparagement"? After a similar conflict of interest unfolded in
Britain, their entire Ministry of Agriculture was dissolved and an
independent Food Safety Agency was created, whose sole responsibility is
to protect the public's health. Until we learn from Britain's lesson, and
until the USDA stops treating this as a PR problem to be managed instead
of a serious global threat, millions of Americans will remain at risk.
Michael Greger, MD, is a graduate of the Cornell University
School of Agriculture and the Tufts University School of Medicine. Dr.
Greger has been speaking publicly about Mad Cow disease since 1993. He
debated National Cattlemen's Beef Association Director Gary Weber
before the FDA and was invited as an expert witness at the infamous
Oprah Winfrey "meat defamation" trial. He has contributed to many
books and articles on the subject, continues to lecture extensively,
and currently coordinates the Mad Cow disease website for the Organic
Consumers Association. Dr. Greger can be reached for media inquiries
at (617) 524-8064 or
(Full text of specific articles available by emailing
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Michael Greger, M.D.
Chief BSE Investigator for Farm Sanctuary
Mad Cow Coordinator for the Organic Consumers Association
185 South St #6
Boston, MA 02130
For periodic updates on the Mad Cow crisis send a blank email to
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