MAD COW DISEASE, PART 1

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RACHEL'S ENVIRONMENT & HEALTH WEEKLY #606 .

 

.. ---July 9, 1998--- .

 

.. HEADLINES: .

 

.. MAD COW DISEASE, PART 1 .

 

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MAD COW DISEASE, PART 1

 

 

 

In 1985, cows in Britain began to die of a mysterious ailment

 

that no one had ever seen before. The symptoms were strange. At

 

first the cows staggered and drooled, their ears twitching. Then

 

they began to show signs of fear, grinding their teeth, acting

 

aggressively toward other animals. Soon they died. Farmers named

 

the condition " mad cow disease " and the name stuck.

 

 

 

The disease is now known formally as " bovine spongiform

 

encephalopathy " or BSE for short. BSE is one of a small family of

 

diseases called transmissible spongiform encephalopathies, or

 

TSEs. TSEs destroy neurons, the main nerve cells in the brain,

 

creating holes that leave the brain resembling a sponge (thus

 

" spongiform " ). BSE, like the other TSEs, is an infectious

 

disease, meaning that it can be transmitted from one cow to

 

another.

 

 

 

During the 13 years since it first appeared, mad cow disease

 

has killed more than 167,000 cows in Britain[1] and many more

 

became infected but were slaughtered for food before symptoms

 

appeared. Symptoms take an average of 5 years to show up after a

 

cow is infected. Until the late 1990s, there was no test that

 

could detect whether a cow was infected -- only the appearance of

 

symptoms and microscopic examination of the brain could provide a

 

definitive diagnosis. (Even today, tests require brain tissue, so

 

they cannot be conducted on live animals.) British-type BSE has

 

now been observed in cows in Switzerland, the Netherlands,

 

Ireland, Portugal, France, Oman and the Falkland Islands. To

 

date, the disease has not been observed in cows in the U.S.

 

 

 

When the disease first struck in Britain in 1985, health

 

authorities insisted that British beef was safe to eat. For 10

 

years they defended that position aggressively, despite mounting

 

evidence to the contrary. Then in 1996, the official story

 

changed suddenly and the public was stunned. A panel of

 

government scientists told Parliament in 1996 that the " most

 

likely explanation " for 10 cases of a new TSE disease in humans

 

was that BSE had moved from cows into people. That explanation is

 

now widely accepted by most scientists, though airtight evidence

 

remains elusive.

 

 

 

By the time of the stunning announcement in 1996, some

 

British experts calculated that more than a million infected cows

 

had already been consumed in Britain.[2]

 

 

 

In humans, the BSE-like disease is called " new variant

 

Creutzfeld-Jacob disease, " or nvCJD for short. Creutzfeld-Jacob

 

disease (CJD) is a member of the TSE family, a brain-destroyer.

 

CJD has been recognized for a long time as a rare disease of the

 

elderly -- very similar to Alzheimer's disease -- but nvCJD is

 

different. It has somewhat different symptoms, a different

 

pattern of disintegration in the brain, and it strikes young

 

people, even teenagers. Between 1995 and early 1998, at least 23

 

people died of nvCJD in Britain and at least one in France,[3] the

 

oldest of them age 42 and the youngest 15.

 

 

 

In January 1997, British epidemiologists tried to estimate

 

how large the outbreak of nvCJD might become. They concluded that

 

the data were not sufficient to allow a precise estimate:

 

somewhere between 75 people and 80,000 people would eventually

 

die of the new disease, they estimated.[4] Only time will tell.

 

More precise estimates of the size of the problem are not

 

possible because no one knows for sure how long nvCJD

 

" incubates, " how much time elapses between infection and the

 

appearance of symptoms.

 

 

 

An excellent recent book by Sheldon Rampton and John Stauber,

 

MAD COW U.S.A.--CAN THE NIGHTMARE HAPPEN HERE? tells the story of

 

the emergence of mad cow disease in Britain, and the scientific

 

and political battles that have ensued.[5] Despite the evocative

 

title, the book is thoroughly-documented and carefully-written.

 

Without oversimplifying the details, the book recounts a

 

complicated story of medical discoveries, strongarm tactics by

 

the beef industry, and waffling and coverup by governments on

 

both sides of the Atlantic -- yet it reads as easily as a

 

detective story. As a piece of science writing -- a description

 

of science as it plays out in the real world -- the book is an

 

impressive accomplishment. By the end, the reader has absorbed

 

several important lessons about public health policies distorted

 

by big money, and about very serious threats to our first

 

amendment right of free speech. Rampton and Stauber show that the

 

U.S. beef industry will go to almost any lengths to try to

 

prevent a public discussion of " mad cow " and the steps that the

 

U.S. government still needs to take to prevent this disease from

 

becoming an American problem.

 

 

 

In a nutshell: Mad cow disease developed because of a

 

little-known but very-widespread modern agricultural practice --

 

farmers feeding dead cows to their cows, thus turning a

 

vegetarian species into meat-eaters.

 

 

 

In Britain and the U.S., when a cow is slaughtered, about

 

half of the animal cannot be sold for human uses -- the hide,

 

bones, entrails, hooves, horns, fat, gristle and tough membranes

 

are, by law, not permitted to be used in food. Obviously

 

something else has to be done with these parts, to avoid creating

 

a public health hazard.

 

 

 

Then there are " downer cows " that must be dealt with. Cows

 

that cannot stand up, cows that collapse, and cows that die

 

mysteriously are called " downers. " Every year in the U.S. about

 

100,000 cows die of unknown causes. One day they are alive and

 

the next day they are dead, and no one knows why. Something must

 

be done with their carcasses.

 

 

 

In addition to downer cows there are thousands of pigs,

 

horses, chickens, and sheep that die of unknown causes each year.

 

To prevent public health problems, they must be disposed of. Then

 

there is road kill -- deer, elk and other large mammals killed by

 

motor vehicles.

 

 

 

In the U.S. all of these animals and animal parts end up at

 

280 " rendering " plants where they are ground up and boiled down.

 

(The British call such plants " abbatoirs. " ) Up until the 1960s,

 

the fat from rendering plants was generally used to make soap.

 

But the invention of detergents, derived from petroleum, greatly

 

reduced the demand for soap. As a result, the rendering industry

 

had to develop new markets for its products. They hit on animal

 

feed, and it became a great commercial success.

 

 

 

From the 1960s through the mid-1990s, rendering plants dried

 

their rendered products, ground them into the consistency of

 

brown sugar, and sold them for animal feed. Feed mills then mixed

 

these animal by-products into various feed formulations -- about

 

one-third for cattle, one-third for pigs and chickens, and

 

one-third for pets.

 

 

 

Unfortunately, some of the animals sent to rendering plants

 

(or abbatoirs) are sheep killed by a disease called " scrapie. "

 

Scrapie is another TSE, a member of the same family as BSE, CJD,

 

and nvCJD -- one of those diseases that eats holes in the brain

 

and invariably kills its victims. Scrapie takes its name from the

 

way sheep act once they get the disease -- they rub up against a

 

fence or a barn until they scrape away their wool, leaving raw

 

wounds. Then they die.

 

 

 

Scrapie has been a well-known, though mysterious, disease of

 

sheep for at least 200 years, but only recently have

 

scrapie-infected sheep been fed to cows. Scientists who study mad

 

cow disease believe that the illness crossed the species barrier

 

from sheep to cows through contaminated feed. Indeed, the British

 

in 1988 banned the practice of feeding animal carcasses to other

 

animals and within seven years new cases of mad cow disease

 

diminished quite dramatically from 900 to 1000 per week to 280 to

 

300 per week.[6]

 

 

 

The U.S., however, has been slow to act. Scrapie is

 

well-established among sheep in this country. From October, 1988,

 

to June, 1989, scrapie was diagnosed in 52 flocks of sheep in 20

 

states.[5,pg.104] Clearly, there was ample reason to ban the

 

feeding of animal carcasses to animals in this country when the

 

British took that action in 1988. However, the beef industry, and

 

the rendering and feed industries, have generally opposed such

 

precautionary measures.

 

 

 

TSEs have a very long incubation period. In cows, BSE takes

 

three to eight years (average, five years) from the time of first

 

infection to the appearance of symptoms shortly before death. CJD

 

in humans has an incubation period of 10 to 40 years. Thus, by

 

the time symptoms of BSE appear, many cows are likely to be

 

carrying the infection silently. This was confirmed earlier this

 

year in Switzerland when tests of brain tissues from 1761 cows

 

revealed 8 infected animals without any symptoms, for a " silent "

 

infection rate of 4.5 per 1000. This is 100 times as high as the

 

rate of Swiss cows showing symptoms.[7] If this rate holds for

 

Britain, it means that today there are about 460,000 British cows

 

infected -- but symptom-free -- in a total herd of roughly 11

 

million.

 

 

 

TSE diseases are characterized by a long incubation period,

 

and they are always fatal. Furthermore, the infectious agent is

 

incredibly resistant to deactivation. Cooking infected meat, or

 

even rendering it at high temperature, does not completely

 

eliminate its infectivity. Animals get TSEs by eating infected

 

animals or parts of infected animals, especially nerve tissues.

 

 

 

TSE diseases have now been identified in sheep, pigs, goats,

 

cattle, deer, elk, mink, mice, hamsters, guinea pigs, domestic

 

cats, puma, cheetah, eland, kudu, Arabian oryx, myland,

 

marmosets, macaques, chimpanzees and humans. In addition, a TSE

 

has been reported in ostriches in a German zoo.[8]

 

 

 

Thus one might think the U.S. Food and Drug Administration

 

(FDA) would prohibit the feeding of any animals to any other

 

animals, as the British did in 1988. But that is not what the FDA

 

has done. Under pressure from the beef, rendering, and feed

 

industries, in 1997 FDA only prohibited the feeding of ruminants

 

and mink to ruminants.[1,8] Ruminants are animals that chew their

 

cuds, including cattle, sheep, goats, deer and elk. Mink are

 

included in the ban because they can get a TSE similar to mad cow

 

disease.

 

 

 

FDA is still allowing the feeding of pigs to other animals,

 

and the feeding of blood and gelatin from rendering plants to all

 

animals. For example, many calves in the U.S. are being raised on

 

a diet of dried blood taken straight from rendering plants. Pigs

 

and chickens are still being fed rendered animal products. There

 

are sound scientific arguments why this policy represents a form

 

of Russian roulette being played with the health of the American

 

public. Given that we are dealing with infectious diseases that

 

invariably kill, the precautionary principle (see REHW #586)

 

seems the only appropriate policy.

 

 

 

More next week.

 

--Peter Montague

 

(National Writers Union, UAW Local 1981/AFL-CIO)

 

 

 

=========

 

 

 

[1] Michael Hansen, " The Reasons Why FDA's Feed Rule Won't

 

Protect Us from BSE, " GENETIC ENGINEERING NEWS (July, 1997), pgs.

 

4, 40. See also Lawrence K. Altman, " F.D.A. Proposal Would Ban

 

Using Animal Tissue in Feed, " NEW YORK TIMES January 3, 1997, pg.

 

A14, which says BSE has affected 165,000 British cows.

 

 

 

[2] John Darnton, " Britain Ties Deadly Brain Disease to Cow

 

Ailment, " NEW YORK TIMES March 21, 1996, pgs. A1, A7.

 

 

 

[3] Associated Press, " Clues Found in Brain-Killing Process, " NEW

 

YORK TIMES February 10, 1998, pg. F7.

 

 

 

[4] S.N. Cousens and others, " Predicting the CJD Epidemic in

 

Humans, " NATURE Vol. 385 (January 16, 1997), pgs. 197-198. See

 

also, David C.G. Skegg, " Epidemic or false alarm? " NATURE Vol.

 

385 (January 16, 1997), pg. 200.

 

 

 

[5] Sheldon Rampton and John Stauber, MAD COW U.S.A. COULD THE

 

NIGHTMARE HAPPEN HERE? (Monroe, Maine: Common Courage Press,

 

1997). ISBN 1-56751-111-2. Available from Common Courage Press,

 

Box 702 Monroe, Maine 04951. Telephone (207) 525-0900; fax: (207)

 

525-3068.

 

 

 

[6] John Darnton, " Fear of Mad-Cow Disease Spoils Britain's

 

Appetite, " NEW YORK TIMES January 12, 1996, pgs. A1, A8.

 

 

 

[7] Debora MacKenzie, " BSE's hidden horror, " NEW SCIENTIST (June

 

13, 1998), pg. 4.

 

 

 

[8] [Michael Hansen], " Consumers Union's Comments on Docket No.

 

96N-0135, Sustances Prohibited for Use in Animal Food or Feed;

 

Animal Proteins Prohibited from Ruminant Feed, Draft Rule, " April

 

28, 1997. Available from Michael Hansen, Consumer Policy

 

Institute, Consumers Union, 101 Truman Avenue, Yonkers, NY

 

10703-1057; telephone (914) 378-2000.

 

 

 

 

 

Descriptor terms: mad cow disease; emerging diseases;

 

creutzfeld-jacob disease; new variant creutzfeld-jacob disease;

 

nvcjd; cjd; great britain; consumers union; bse; tse;

 

transmissible spongiform encephalopathies; sheldon rampton; john

 

stauber; scrapie; britain; michael hansen;

 

 

 

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