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MAD COW DISEASE,
For the past several years, the U.S. Food and Drug Administration (FDA) has been considering ways to prevent an epidemic of "mad cow disease" in the U.S. In Britain, where the disease has killed 170,000 cows and at least 24 people since 1985, the beef industry has been crippled and confidence in government has plummeted because no one took adequate measures to control the disease. Additional human deaths are now expected in Britain because millions of people ate contaminated beef for a decade before authorities acknowledged that mad cow disease could endanger public health. (See REHW #606, #607.) Could such a thing happen in the U.S.?
When animals are slaughtered for human food, at least half of the carcass --hide, hooves, entrails, and so forth --cannot be sold for human food and must be sent to a "rendering" plant where it is ground up, boiled down, dried into the consistency of brown sugar and sold as feed for cows, pigs, chickens, and pets. Cows --vegetarians by nature --can become infected by mad cow disease when they are forced to eat parts of other infected animals.
June 5, 1997, FDA issued a rule making it illegal for rendered animal parts from ruminants or mink to be fed to ruminants. Ruminants are animals that chew their cuds --cattle, sheep, goats, deer and elk, among others. Mink are included in the FDA's ban because they can get a disease similar to mad cow disease.
A small group of scientists, led by Michael K. Hansen of Consumers Union, argues that the FDA ban does not go far enough to protect public health, and that FDA's rule is "not scientifically defensible."[1] Hansen wants a ban on all animal feed containing anything derived from rendered mammals. Consumers Union publishes CONSUMER REPORTS magazine.
FDA says its ban is adequate because no cows in the U.S. have ever been confirmed with mad cow disease, nor is there evidence that any humans in the U.S. have been affected. However, last week we reviewed indirect evidence indicating that some cows in the U.S. may already have mad cow disease and that some people in the U.S. may already have a human version of the disease. In Britain, mad cow disease is thought to have infected some people with a variant of an age-old, but very rare, disease called Creutzfeld-Jakob disease, of CJD for short. In this country, there is some evidence that CJD may not be as rare as was once thought because some cases of CJD may have been misdiagnosed as Alzheimer's disease. (See REHW #607.)
Mad cow disease is one of a family of diseases called transmissible spongiform encephalopathies, or TSEs for short. In sheep, the disease is called scrapie; in deer and elk it is called chronic wasting syndrome. In cows, it is called BSE [bovine spongiform encephalopathy] and in mink it is TME [transmissible mink encephalopathy].
TSE diseases all have similar characteristics: they attack the central nervous system, causing disintegration of the brain; they have a long incubation period --months or years (even decades) can pass between the initial infection and the time when symptoms appear; TSEs are invariably fatal; and they are transmitted by eating animals or animal parts, especially brains and spinal cords.
TSEs are now thought to be caused by a protein called a prion (pronounced PREE-on). Prions are normal proteins, present in all mammals and some non-mammalian species such as salmon and ostriches. According to the prion theory of disease, some prions can fold abnormally and then they can kill nerve cells. Furthermore, according to the theory, abnormal prions can cause normal prions to fold abnormally, thus causing a chain reaction leading eventually to disease and death.[2]
Prions are remarkably hardy. They are not destroyed by the digestive system of humans or other animals. And they are very heat resistant. A scientific committee of the European Union says that heating prions to 271 degrees Fahrenheit (133 Celsius) under three atmospheres of pressure will deactivate most, but not necessarily all, of them. Prions also resist destruction by ultraviolet light and by radiation, and they are not affected by prolonged immersion in formalin, a potent disinfectant made from formaldehyde and alcohol.[3] Prions are hard to stop.
Under FDA's rule, ruminants can be fed to pigs and pigs can be fed to ruminants. Under the rule, even ruminants that are known to be infected with a TSE can be fed to pigs. FDA allows this because, the agency says, no "naturally occurring" TSE has ever been confirmed in pigs. However, Dr. Hansen notes that British researchers have managed to infect pigs with a TSE by exposing them to high doses of contaminated brains from cattle.[4] This does not answer the question whether pigs can be infected through their normal diet, but it indisputably establishes that pigs, like many other species, are susceptible to TSEs.
Hansen offers evidence that some pigs in the U.S. may be infected with a TSE.[5] In 1979, Dr. Masuo Doi, a U.S. Department of Agriculture (USDA) hog inspector, began noticing pigs with central nervous system (CNS) disorders arriving at a swine slaughterhouse, the Tobin Packing Plant, in Albany, New York. Because there was no single source of the animals, and because the Tobin plant did not routinely deal in diseased animals, Dr. Doi suspected that the symptoms he was observing might be present in pigs nationwide.[6] During a 16-month period, Dr. Doi observed CNS symptoms in 106 pigs, taking careful notes and retaining tissue samples, including brains. Researchers examined the brains of the 106 pigs and found telltale "spongiform damage" --holes in the brain tissue --in only one of the 106. They did find other brain damage that occurs in TSE diseases --so-called "glial changes" in brain cells --in 40% of the animals. Dr. Doi, and Dr. Langeheinreich, the pathologist who examined the brain tissues, both say they believe they were dealing with a single disease in all the pigs. Dr. Clarence Gibbs, the leading expert on TSEs at the National Institutes of Health, has said he believes all the pigs had the same disease, based on behavioral abnormalities evident in motion pictures taken while the pigs were alive.
There are 83 million pigs slaughtered in the U.S. each year.[6] They are killed at an average age of only 5 months --long before symptoms of a TSE would ordinarily become apparent.[1] Therefore, if pigs were infected with a TSE, they still might end up in food products for humans and in animal feed.
Even if a pig had the behavioral symptoms of a TSE disease, it might not be noticed by USDA inspectors. To see the symptoms of such disorders, one must observe an animal in motion. The way they walk, turn corners, and hold their tails and heads can all be important clues to their condition. Most pigs are so jammed into pens with other pigs that they have no room to move. If the animals are not in motion, symptoms of TSEs (or other CNS disorders) can go unnoticed. At present, USDA observes only 5% to 10% of pigs while they are in motion.[6] Thus USDA's inspection program seems inadequate to detect symptoms of TSE diseases in pigs. And, as we have noted, even if a pig were identified with a TSE, FDA's rule would allow its infected carcass to be fed to all non-ruminant animals, including pets, chickens, fish, and pigs.
Do humans who eat pork and other pig products have high rates of CJD, the human TSE associated with mad cow disease in Britain?
There have been two epidemiological studies on this point.[7,8] Both were suggestive, though not definitive. The first study, in 1973, examined 38 patients with Creutzfeld-Jakob disease. The control group consisted of the nearest relatives of the CJD patients, often their spouses. These controls then selected a friend of the patient of the same age and sex to act as a second control.
The study revealed that this group of people had an unusual diet. More than one-third of the CJD patients ate brains "and the great majority of patients had a specific preference for hog brains," the authors wrote.[7] One-third of the control group also ate brains, but not necessarily hog brains. Obviously the control group, composed of close relatives and close friends, shared dietary habits with the patients, reducing the power of the study to discern differences between the two groups.[7]
The second study, in 1985, compared 26 patients with Creutzfeld-Jakob disease with 18 of their family members and 22 other people selected from a hospital population.[8] Compared to the control group, the CJD patients had an unusually high consumption of roast pork, ham, hot dogs, pork chops, smoked pork, and scrapple. Scrapple is made by adding cornmeal to the liquid derived by boiling pig bones and meat (usually from the head, feet and internal organs). Compared to controls, CJD patients also had an excess consumption of roast lamb, rare meats [meaning not thoroughly cooked], and raw oysters and clams.
Could TSE-infected meat enter the human food chain from other sources besides pigs? The state of Colorado requires deer hunters to turn in the heads of any deer they kill. In 1996, 6% of the deer in northeastern Colorado were found to have a TSE. In 1997, 4% of the deer there had a TSE.[9] Diseased deer in Colorado are usually incinerated or buried in a landfill (where the prions remain infective for an unknown period). However, if any diseased roadkill deer were sent to a rendering plant, they could become animal feed for pigs and chickens.
It is not known at this time whether chickens can become infected by TSE diseases. However, even if it turns out that chickens cannot get a TSE disease themselves, they still might carry such a disease if it were in their feed. As we have noted, the FDA rule allows chickens to be fed rendered animal protein even if it is known to be infected with TSE diseases. Dr. Clarence Gibbs, Acting Chief of the Laboratory of Central Nervous System Studies at the National Institutes of Health, testified before Congress January 29, 1997, saying that bone meal derived from infected rendered animals has been fed to chickens. "Poultry would be expected to shed massive quantities of the infectious amyloid [prion protein] in their feces. Chicken manure is widely used as fertilizer on vegetable crops. This means that vegetarians might be at risk," Dr. Gibbs testified.[1]
--Peter Montague (National Writers Union, UAW Local 1981/AFL-CIO)
MAD COW DISEASE, PART 2
Mad cow disease appeared for the first time in Britain in 1985. Since that time it has killed roughly 170,000 cows in Britain, and it has spread to humans.[1] In humans the disease is called "new variant Creutzfeld-Jakob disease," or nvCJD for short. At this point nvCJD has killed 24 people in Britain and one in France. More human deaths are expected in Britain[2] because several million people ate diseased beef before the British government (or the beef industry) acknowledged that mad cow disease could infect people.
From a U.S. perspective, the obvious question is, How can an outbreak of mad cow disease be prevented here?
Mad cow disease is a member of a family of rare diseases called transmissible spongiform encephalopathies, or TSEs. TSEs have different names in different animals (for example, scrapie in sheep, chronic wasting syndrome in deer and elk, and bovine spongiform encephalopathy or BSE in cows). However all TSEs share a few common features: they attack the central nervous system, causing disintegration of the brain; they have a long incubation period between the time when infection first occurs and the appearance of symptoms; TSEs are always fatal; and they are transmitted by the eating of animals or animal parts, especially brains and spinal cords.
TSEs are now thought to be caused by a unique disease agent, called a prion (pronounced PREE-on). A prion is simply a particular kind of protein. All mammals have prions, and some non-mammalian species have them as well. Prions are normal.
According to modern biology, a prion should not be able to reproduce itself, and therefore should not be able to cause disease, because prions contain no DNA. Without DNA, reproduction should not be possible. However, it is now becoming widely accepted that prions do reproduce themselves and do cause disease. Somehow a normal prion goes bad --it gets folded into an abnormal shape and in its abnormal shape it can destroy nerve cells in the central nervous system. The abnormal prions also cause other nearby prions to become folded into the same shape, thus creating more abnormal prions by a domino effect. After a long period of time (months or years, or even decades) the symptoms of disease appear, followed a few weeks or months later by death. Thus animals and humans can be carrying an infectious prion disease for months or years without showing any symptoms.
The prion theory of disease is still not accepted by 100% of the scientific community, but the inventor of the theory, Stanley B. Prusiner of the University of California at San Francisco, received the Nobel Prize for his work in 1997.[3]
In this country, the government agency with primary responsibility for preventing an outbreak of mad cow disease or its human variant, nvCJD, is the U.S. Food and Drug Administration (FDA).
The FDA in 1997 issued a rule declaring it illegal for farmers to feed animal protein from ruminants or mink to other ruminants --a preventive step that had been taken by the British government in 1988. Ruminants are animals that chew their cuds, including cattle, sheep, goats, deer and elk. Mink are included in the FDA's ban because they can get a TSE similar to mad cow disease.
When cows, pigs, and chickens are slaughtered, much of the animal cannot be used for food and is sent to a rendering plant to be ground up, boiled down, dried to the consistency of brown sugar and sold as feed for cows, pigs, chickens, and pets. It is this rendered "animal protein" derived from ruminants (and mink) that FDA has banned from feeding to ruminants.
The FDA's ruminant-to-ruminant ban still allows animal protein of all kinds to be fed to pigs and chickens, and it allows animal protein derived from pigs and chickens to be fed to ruminants. The FDA ban also allows blood and gelatin derived from ruminants to be fed to other ruminants. In the U.S., many newborn calves are fed a high-protein diet consisting mainly of dried blood. Blood cells carry prions just as nerve cells do.[4]
A small group of scientists, led by Dr. Michael Hansen of Consumers Union, has challenged the adequacy of FDA's ruminant-to-ruminant rule.[5] They argue that the FDA ban does not go far enough, "does not adequately protect human health, and is not scientifically defensible."[6] Consumers Union is the publisher of CONSUMER REPORTS magazine.
Scientists on both sides of the controversy agree that mad cow disease probably developed in Britain in one of two ways. Possibly cows ate parts of sheep that had been infected with the TSE called scrapie, and the scrapie, once in cows, evolved into mad cow disease. Or, alternatively, a prion spontaneously went bad (via genetic mutation of the gene that produces normal prions) in a cow, and that cow was fed to other cows, which were fed to other cows until the disease was amplified into an epidemic. In either case, it was cows (which are vegetarians by nature) being forced to eat animals that created the problem.
FDA officials say they are confident that their ruminant-to-ruminant ban has prevented, and will continue to prevent, an epidemic of mad cow disease in this country because (a) mad cow has never been observed in cows in the U.S., and (b) Creutzfeld-Jakob (CJD) disease is not increasing in the U.S.[7] If mad cow were occurring in U.S. cows, some form of CJD should be increasing, and it isn't, the FDA argues.
Michael Hansen of Consumers Union offers evidence that the government may be wrong on both counts. Here are his arguments:
Mad cow may have already appeared in U.S. cows. Hansen offers evidence from seven studies that some "downer" cows may have a form of mad cow disease, though with symptoms somewhat different from those in British cows. Downer cows are cows that cannot stand up, cows that collapse, and cows that die mysteriously. About 100,000 cows die each year in the U.S. with "downer" symptoms, and most of them end up in rendering plants, turned into animal feed.
In 1961, an outbreak of transmissible mink encephalopathy (TME) --a brain-destroying TSE of mink --occurred on six mink farms in Wisconsin. Because all the farms used the same ready-mix feed which came from the same feed plant, investigators assumed that the feed was the source of the infectious agent.[8] Two years later, in 1963, an outbreak of TME occurred on two more Wisconsin mink farms. Based on the 1961 outbreak, scientists suspected feed and they examined the two farms' feed records carefully. They learned that "downer" cows from farm A had been fed to mink on Farm A and Farm B. The researchers wrote, "Since mink on both farms developed the disease almost simultaneously, we believe this feed component has to be incriminated."[9]
In 1985 an outbreak of TME occurred on a mink ranch in Stetsonville, Wisconsin. Dr. Richard Marsh of the University of Wisconsin investigated and found that the mink had been fed 95% downer cows and 5% horse meat.[10] When brains from infected mink were injected into two calves, within 19 months both calves had a bovine TSE but they did NOT exhibit the symptoms of Britain's mad cows. The Stetsonville cows simply became lethargic and then fell over. In other words, they exhibited typical "downer cow" symptoms. When brains from these cows were injected into mink, the mink got TME, confirming the kind of disease that had killed the cows. Marsh and his colleagues concluded, "These results suggest the presence of a previously unrecognized scrapie-like infection in cattle in the United States."[10]
Marsh's cattle inoculation experiments have been repeated and, again, mink TME was transmitted to cows and back to mink and the cows exhibited "downer" symptoms, nothing like British mad cow disease.[8] Furthermore, in 1979 U.S. Department of Agriculture researchers in Mission, Texas, inoculated 10 cows with sheep scrapie. Three of the 10 cows developed neurological symptoms, but they were more like "downer cow" syndrome than British mad cow disease: "progressive difficulty in rising, a stiff-legged gait, incoordination, abnormal tail position, disorientation, and terminal recumbency [lying down]," according to Dr. Clarence Gibbs, Acting Chief of the Laboratory of Central Nervous System Studies at the National Institutes of Health.[11] Ten years later, when a test for mad cow disease became available, Dr. Gibbs confirmed a bovine TSE disease in the three cows, whose brains had been preserved.[11] Dr. Gibbs concluded, "Susceptibility of cattle to scrapie further suggests the possibility that sporadic cases of BSE [mad cow disease] may have occurred in the United States under the clinical picture of the downer cow syndrome...."[11]
After Gibbs confirmed that the Mission, Texas cows had indeed died of a TSE, the U.S. Department of Agriculture repeated the experiments at Ames, Iowa under the direction of Randall Cutlip.[12] Dr. Cutlip described the results: "All calves kept longer than one year became severely lethargic and demonstrated clinical signs of motor neuron dysfunction that were manifest as progressive stiffness, posterior paresis [partial paralysis], general weakness, and permanent recumbency [lying down]." In other words, cows infected with a sheep TSE had all the signs and symptoms of downer cows.
Thus Hansen argues, there is considerable evidence that a TSE has been present in some U.S. cattle for several decades.
But if mad cow disease is already present in some number of cows in the U.S., where are the human victims? People should be getting some form of CJD [Creutzfeld-Jakob disease], and this disease is thought to be vary rare and not increasing in the U.S. population. So where are the victims?
Hansen argues that CJD may be more prevalent in the U.S. population than is presently thought. The official figures say that CJD is exceptionally rare --one case in every million people. In the U.S. this would mean there are 250 CJD cases at any given time. Hansen points to two studies in which people diagnosed with Alzheimer's were examined after death. In one study, among 54 presumed Alzheimer's victims, 3 (or 5.5%) were found to actually have CJD.[13] A Yale University study of 46 victims of Alzheimer's found that 6 (or 13%) actually died of CJD, not Alzheimer's.[14] There are 2 million people with Alzheimer's in the U.S.[8] If 5.5% of them actually have CJD, there are 110,000 cases of CJD in the U.S., not 250 cases. If 13% of the 2 million have CJD, then there are 260,000 cases of CJD in the U.S., not 250. If even 1% of the 2 million had CJD, it would mean there was an epidemic of 20,000 cases of CJD masquerading as Alzheimer's. Thus the FDA's argument that CJD is very rare, and not increasing, needs to be re-examined.
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