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Could Mad Cow Disease
Already be Killing Thousands of Americans Every Year?
by Michael Greger, M.D.
January 7, 2004
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.[4] 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.[5] 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.[6] The announcement of their deaths,
released on March 20, 1996 (ironically, Meatout Day[7]), reversed the
British government's decade-old stance that British beef was safe to
eat.[8] It is now considered an "incontestable fact" that these
human deaths in Britain were caused by Bovine Spongiform Encephalopathy
(BSE), or Mad Cow disease.[9] 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[10]
at temperatures hot enough to melt lead.[11] 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 scrapie.[12]
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 sporadic CJD.
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.[13] 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.[14] Hundreds of confirmed cases of the sporadic form of
Creutzfeldt-Jakob disease, however, arise in the United States every
year,[15] 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.[16] 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 all.
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."[17] 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
disease]..."[18]
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.[19] "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.[20] 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.[21] Hundreds of "mad sheep" were found in the U.S. in 2003.[22]
Scrapie remains such a problem in the United States that the USDA has
issued a scrapie "declaration of emergency."[23] Maybe
some cases of sporadic CJD in the U.S. are caused by sheep meat as
well.[24]
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[25]--and hundreds of
thousands of downer pigs, too sick or crippled by injury to even walk,
arrive at U.S. slaughterhouses every year.[26]
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.[27] 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).[28]
Sporadic CJD has also
been associated with weekly beef consumption,[29] as well as the
consumption of roast lamb,[30] veal,venison, brains in general,[31] and,
in North America, seafood.[32,33] The development of CJD has also,
surprisingly, been significantly linked to exposure to animal products in
fertilizer,[34] sport fishing and deer hunting in the U.S.,[35] and
frequent exposure to leather products.[36]
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.[37] 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.[38]
Dateline NBC quoted D. Carleton Gajdusek, the first to be awarded a Nobel
Prize in
Medicine for his work on prion diseases,[39] as saying, "it's got to be in
the pigs as well as the cattle. It's got to be passing through the
chickens."[40] 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."[41]
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[42]). 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 guaranteed.
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."[43] In the Nineties, Switzerland had the
highest rate of Mad Cow disease in continental Europe, and their rate of
sporadic CJD doubled.[44]
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.[45] 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,[46] a
rise similar to the one in Europe could be missed.[47] 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,[48] five times the expected rate
was found to be associated with cheese consumption in Pennsylvania's
Lehigh Valley.[49] A striking increase in CJD over expected levels was
also reported in Florida[50] and New York (Nassau County)[51] with
anecdotal reports of clusters of deaths in Oregon[52] and New Jersey.[53]
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.[54]
The most frequent
misdiagnosis of CJD among the elderly is Alzheimer's disease.[55] Neither
CJD nor Alzheimer's can be
conclusively diagnosed without a brain biopsy,[56] 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.[57]
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.[58] In younger victims, CJD is more often misdiagnosed as
multiple sclerosis or as a severe viral
infection.[59]
Over the last 20 years
the rates of Alzheimer's disease in the United States have
skyrocketed.[60] According to the CDC, Alzheimer's Disease is now the
eighth leading cause of death in the United States,[61] afflicting an
estimated 4 million Americans.[62] 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.[63] 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.[64]
Nobel Laureate Gajdusek,
for example, estimates that 1% of people showing up in Alzheimer clinics
actually have CJD.[65] At Yale, out of a series of 46 patients clinically
diagnosed with Alzheimer's, six were proven to have CJD at autopsy.[66] 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.[67] An informal survey of neuropathologists registered a
suspicion that CJD accounts for 2-12% of all dementias in general.[68] 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.[71] Although only a few hundred cases of sporadic CJD are officially
reported in the U.S. annually,[72] hundreds of thousands of Americans die
with dementia every year.[73] 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.[74] 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
http://organicconsumers.org/madcow/GregerBSE.cfm), and should
immediately enact an active national surveillance program for CJD.[75]
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.[76] The petition was denied.[77]
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.[78] But CJD
is so often misdiagnosed, and autopsies are so infrequently done, that
this system may not provide an accurate assessment.[79]
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."[80] "The chance of losing an important case is high."[81]
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.[82] 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.[83] Although one reason autopsies are rarely performed on
atypical dementia cases is that medical professionals are afraid of
catching the disease,[84] 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.[85]
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."[86] 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."[87] "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
crisis."[88]
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."[89] 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."[90]
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."[91]
Plant sources of protein
for farm animals can cost up to 30% more than cattle remains.[92] 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 "activists."[93]
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?[94] Or
Alison Harrison, former director of public relations for the Cattlemen's
Association, as her official spokeswoman?[95] 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"?[96] 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,[97] 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
mhg1@cornell.edu.
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http://www.organicconsumers.org/madcow/BSE7601.cfm
--
Michael Greger, M.D.
Chief BSE Investigator for Farm Sanctuary
http://www.nodowners.org
Mad Cow Coordinator for the Organic Consumers Association
http://www.organicconsumers.org/madcow.htm
(617) 524-8064
(206) 312-8640
mhg1@cornell.edu
185 South St #6
Boston, MA 02130
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