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International Meat Crisis



Public health experts agree that we are on the verge of an epidemic of massive proportions. Some say that it may, within a decade, become worse than the AIDS crisis. This is the story of mad cow disease.


It all began in the Fore tribe, living in the jungle near Papua, southern New Guinea. That is where the modern epidemic, known as mad cow disease, got its start.

It was an area unexplored by Westerners until the second half of the twentieth century.

Although they had heard something about it a decade earlier, it was not until the early 1950s that scientists had opportunity to puzzle over a strange brain-wasting disease in a tribe in New Guinea. The people there had a tribal ritual dating from the prehistoric past, in which they would eat their relatives, when they died, in order to acquire the mental and physical stamina they had while still alive. Women especially did this in order to increase their fertility. They thought it would help them have more children.

Scientists found that many of the people in this tribe were dying of a mysterious brain disease which they, the nationals, called "Kuru," because it made its victims act very strange before they died. Kuru was killing up to 80 percent of the women in the tribe. (It was known that the women ate far more dead relatives than did the men, who primarily ate beans and sweet potatoes.)

Once the symptoms showed themselves, it took about 16 months before the victim died. There was a progression of tremors and an unsteady gait, followed by slurred speech, joyless laughter, and finally stupor, and death.

No one knew when the disease first started. Because it occurred within families and mostly among women, researchers initially thought that Kuru was inherited genetically. But it has since been established that Kuru is infectious and was transmitted by eating the meat of those dead people.

Peoples in the South Pacific, as well as some other backward areas in the world, have had a long history of cannibalism. But the Fore tribe in New Guinea were remarkably consistent in their eating of dead relatives. This practice, continued for centuries, eventually produced a horrible new disease.

Not only horrible, but unique: The disease was not caused by bacteria, viruses, parasites, fungi, or any other regular means of infection.


In order to understand this, you need to know about prions, BSE, and CJD. First, we will consider prions.

Scientists always used to think that infectious diseases could only be caused by bacteria. But the discovery of prions (pronounced pree-ahns) changed all that. It runs contrary to all the experts had been taught in the universities.

Although prions cause diseases, they are not viruses, bacteria, fungi, or parasites. They are simply proteins! Proteins, by themselves, were never thought to be infectious. Organisms are infectious; proteins are not. Or, at least, they never used to be.

But it is prions which cause mad cow disease.

As we have learned, when researchers began examining the cause of a strange disease in the South Pacific, they could not find any pathological cause.

By the 1970s, a variant of the disease had entered domestic and wild animals in Britain and America; researchers did not recognize the connection of this new disease with the earlier South Pacific disease which attacked humans. Once again, they could not find an infective agent.

It was thought that some kind of extremely tiny virus must be the cause—not a bacteria, not a microbe, but a virus, a sub-microscopic speck of life. For decades, scientists had searched for unusual, atypical infectious agents that they suspected caused some puzzling diseases that could not be linked to any of the "regular" infectious organisms. One possibility was that slow viruses—viruses that spent decades wreaking havoc in their hosts—might be the culprits, and these tiny viruses that were leisurely multiplying are hard to isolate. But the truth finally emerged. Here it is:

Researchers eventually, although reluctantly, accepted the astounding fact that proteins, alone, could be infectious.

These strange proteins, called prions, enter cells and apparently change normal proteins within the cells into prions just like themselves! The normal cell proteins have all the same "parts" as the prions—specifically the same amino-acid building blocks.

There is just one difference: They fold differently. What does that mean?

As soon as a new protein is assembled by other proteins from amino acids within the cell, it folds into a certain pattern. But prions are proteins which fold into a different, incorrect pattern. That little difference renders them deadly.

While other proteins always fold properly, prions are proteins which do not. That little variation makes all the difference—and it results in changes in the brain which produce holes—which look just like the holes in a sponge!

Prions cannot be destroyed by cooking, radiation, or any heat below 800o F.


We have explained what prions are. There are six other special words or phrases which need to be defined:

1 - Bovine spongiform encephalopathy (BSE). This is better known as mad cow disease. It is an infectious and incurable disease which slowly attacks the brain and nervous system of cattle. Spongiform encephalopathy is Latin for "sponge brains."

2 - Spongiform encephalopathies is the name given to this type of disease in various animals and in man.

3 - Scrapie is the form of BSE which is found in sheep. The experts are divided on whether it is harmful to humans. But when the dead animals are fed to cattle, BSE is transmitted. The term comes from the fact that infected sheep will scrape their sides and heads on trees, fence posts, or even barbed wire.

4 - Kuru was once epidemic in a certain tribe in New Guinea, because people liked to eat other people.

5 - Drs. Creutzfeldt and Jakob were researchers in Berlin who, in the early 1920s, gave their names to a strange disease which occurred in one in a million patients. But its utter rarity and the total lack of possible causation permitted the condition to be ignored for decades, until Kuru was discovered.

6 - By late 1994, a handful of people in Britain had died from the same disease, which by that time had been named Creutzfeldt-Jakob disease (CJD). This is the name for the mad cow disease, when it occurs in people. (It is pronounced "Crewtz-felt Yahkob.") Although the disease existed as a rarity prior to the New Guinea research, it did not explode on the world until after Kuru was investigated.

7 - Alzheimer’s disease is a non-spongiform disease. It figures strongly into the present discussion because there is clear evidence that many people, dying in America and elsewhere from Creutzfeldt-Jakob disease, are being misdiagnosed as the victims of Alzheimer’s. More on this later.

In summary:

BSE: Bovine spongiform encephalopathy— This is the animal form of this disease. In cattle, it is called BSE or mad cow disease; in sheep, it is called scrapie.

CJD: Creutzfeldt-Jakob disease—This is the human form of the same disease. In New Guinea, the nationals called it Kuru; in the Western world, it is called CJD. These words will be repeatedly mentioned. You need to understand that BSE is the animal form of the disease and CJD the human form. In popular literature, they are both called "mad cow disease" or simply "mad cow." In this study, when we speak of BSE, CJD, scrapie, or Kuru, we are talking about mad cow disease. The popular use of "mad cow" or "mad cow disease," as the name for the human form, will also be used. (In the U.S., vCJD, or variant CJD is also used. It is essentially the same.)


Whether it be Kuru, BSE, or CJD, patients first show symptoms of mental changes, such as problems with co-ordination, recent memory loss, and slurred speech. Sometimes obvious twitching of muscles can be seen, the facial expression becomes fixed, and the person may stumble and fall over. Over the next few weeks, the person becomes confused and unaware, unable to read or recognize even close relatives. The disease is very similar to Alzheimer’s, yet the cause is very different.

Years later, it has been discovered that BSE in cattle, scrapie in sheep, Kuru in New Guinea, and CJD in the Western world all affect the same part of the brain and nervous system! It is the same disease, whether in animals or man.

Whatever variety of spongiform encephalopathy it may be, this is a disease of the brain and always fatal. There is no known remedy for it. Once a person contracts it, nothing can be done to remove the prions from his body.

Here is an ominous fact about Kuru: Researchers discovered that it could take more than 40 years before the person became visibly ill. The disease bores into the brain and nervous system very slowly; but, once established, it rapidly causes dementia and death. No treatment works. Postmortems show the brain to be sponge-like and full of holes, hence the name "spongiform." Thus the disease can work quietly, insidiously for years before any symptoms develop. How do we know this? Researchers found that Fore tribe women frequently died about 35 years after the last time they ate a dead relative, and some as late as 42 years.


You might wonder how a cannibal disease from one little tribe in New Guinea could get to Europe and America. We are not eating people over here! Here is how it happened:

Scientists eventually brought tissue samples home to America and Britain for careful examination. But they found no antibodies and no disease germs of any kind. There was no microscopic lens in the early 1950s which could have identified the source of infection.

It is now believed that BSE went into the food chain, beginning in Britain and America, when those samples were disposed of. They were either flushed into the sewage system, tossed on garbage heaps, or washed down sink drains.

What those researchers did not know was that there was an infective agent present, one which no heat normally used in laboratories, for cleansing purposes, could kill. Prions which cause BSE and CJD are not destroyed by anything less than 800 degrees F. heat! This is far higher than autoclaving. The only way their sinks, for example, could be cleansed—would be to put them in a high-temperature bake oven for an hour!

Those prions from the samples laid on the ground for a period of time until they were eaten by grazing animals in the Western world. Then they passed into the food chain.

Trillions of prions spread on the ground, waited for some low-grazing animal to come munching toward them. In England, it was first noticed in sheep; in America, with wildlife and sheep. Previous to this time, CJD had been an extremely rare disease, occurring only once in a million cases.

But three facts changed the picture. (1) Tossing out those prions in the early 1950s, which spread an especially virulent form of the disease in the U.S. and Britain and laid the groundwork for what was to come. (2) The feeding of dead, diseased animal carcasses to cows, pigs, and chickens, which we will learn began in the early 1970s. (3) The eating of raw cattle and pig meat, as in the case of those who ate animal glands—a practice which began in the 1960s.


The next outbreak of CJD occurred, not in New Guinea, but from eating raw glandular extract. (Warn your friends who purchase "glandulars" in health-food stores.) In the early 1960s, endocrinologists found that one of the many hormones in the pituitary was the human growth hormone (hGH). They found that it could help dwarfes reach normal heights. Human cadavers were the only known source of hGH, and demand was intense.

So in 1963, the U.S. Government started a National Pituitary Agency, to harvest and distribute the glands. Over the next two decades, roughly 8,200 children were given the hGH through the agency. Similar programs were started in Europe.

But then, in 1984, four of the recipients, now in their 20s, were showing CJD symptoms. The program was stopped on April 20, 1985, after 27,000 children throughout the world had been fed the raw, dead meat. The number who will die from that program is still unknown. Additional deaths are regularly occurring at the present time. CJD can incubate more than 40 years before killing its victim.


In the 1970s, it first appeared in the sheep herds of Britain. British sheepherders called it "scrapie" because the sick sheep had the strange habit of rubbing up against things.

Rams and ewes who had never met a cannibal started exhibiting an odd itch to scrape their heads and hides against fences,—even if the fences were barbed wire. Frankly, the herders said the sheep acted a little crazy.

There were no antibody markers visible at any time during the incubation period, so veterinarians saw no indication of disease. Sick ewes freely gave their illness to their baby lambs who carried the bug straight to human tables.

To this day, there is still no certainty whether sheep with scrapie can infect humans. But we do know that scrapie sheep can, when eaten by them, infect cows—which, when eaten by people, infect them. The facts are hazy, since human dementia deaths in the 1970s were always ascribed to Alzheimer’s.

So now we have the answer to part of the puzzle. In the South Pacific, the disease was transmitted by cannibalism. People were eating their dead relatives. They contracted Kuru.

Later, a new form of cannibalism would be started in the Western world,—that would spread the "civilized" form of Kuru.


Mad cow disease (BSE) has been killing American sheep since the early 1970s, U.S. cows since the mid-1980s, and humans since at least the late 1980s. The reason it hasn’t been made public is that those who had the facts chose to misinterpret them. There is an extremely important reason for this: It could bankrupt the beef industry.

Something was started in 1970 which, in the 21st century, would eventually destroy the U.S. beef industry and kill millions of people in Europe, America, and other nations which import beef from them. Here is what happened:

In 1970, the U.S Department of Agriculture and National Institutes of Health (NIH) collected thousands of scrapie-infected sheep, examined them, and carefully isolated the diseased animals in pens in upstate New York. Once again, they found no bacteria or virus responsible for the problem.

But then, according to Howard F. Lyman, of the U.S. Humane Society (an ex-cattle rancher who was well-aware of what happened), the NIH sold the sick animals at low cost to farmers across the U.S.A., who put them into their herds. It was probably done as a way to help pay for the expensive scrapie research which had been completed. But it was the death knell of the meat industry in America.

Eventually as more sheep got scrapie and could no longer stand on their feet, they were then sold to rendering plants which powdered the carcasses and turned them into animal feed.

Upon eating the prion-loaded animal feed, more livestock contracted BSE. They, in turn, were made into more cattle, sheep, pig, and chicken feed. Which sheepherder wants to spend $500 for an autopsy on a dead animal, when he can sell it for $100?

Did you ever hear of "feeder animals"? They are the animals you eat. In the U.S., there is an enormous industry based on turning cow corpses into animal feed, to be fed to "feeder cattle." The diseased, dead animals are ground up into pellets and, along with a little soy flour, are fed to livestock, to fatten them faster. Because of the high-protein content, the pellets do this quite well.

Here is the procedure: Throughout the nation, whenever cattle, sheep, pigs, chickens, and turkeys die of disease, they are sold to rendering plants. Six-year-old dairy cows and two-year-old egg layers (chickens) are prematurely old and worn out, and are also sold. In recent years, dead and diseased dogs and cats are shipped from humane shelters to the same rendering plants.

At the rendering plant, the whole animal (including the intestines and the manure in it) is ground up and turned into "high-protein pellets." These are then sold as "animal feed" to cattle, sheep, pig, chicken, and turkey ranchers.

When the creatures reach a certain weight, they are then hauled to the slaughterhouses/processing plants (often houses in the same large facility). The animals are killed on fast assembly lines at the slaughterhouses (which, we will learn later in this book, work too quickly to carry out the operation in a clean manner). The processing plants cut, wrap, package, and freeze the meat. It is then shipped to grocery stores, fast-food restaurants, and school lunch programs throughout the nation. Meat is also shipped overseas.

Carefully consider the implications of this: These "feeder cattle" are cattle raised on meat and soy beans. This turns cattle into cannibals! This practice is so solidly entrenched in America that you can actually trade commodity futures on "feeder animals."

The contents of the feed given to the livestock, and the way the animals are slaughtered, are sickening Americans. The powerful livestock industry is doomed to eventually be destroyed by its own practices. This is going to happen, even if they eventually wake up and stop the "feeder animal" business. Among other problems, a major one is that the prions are now in the livestock, and each mother is passing them on to her young at the time of birth.

In summary, this is the formula: If the animal is in bad shape but still can walk, it is sent to the slaughterhouse. If it is too sick to walk or has already died of disease, it is sent to the rendering plant to be turned into pellets to be fed to livestock.


Back in the 1970s in Britain, the sheep that had died of scrapie were rendered into powder and put into animal feed. But the Brits were just copying American frugality, as they used their dead sheep to feed the living ones. No one seemed to be concerned about the fact that the sheep which had died of a mysterious disease were being fed to healthy sheep which did not deserve to die the same way.

So Brits happily ate their sheep, little realizing they were eating cannibals. The curse that destroyed the people in Papua was passing to them and, through livestock shipments, to the whole world.

As the years passed, British sheepherders continued losing more and more sheep to scrapie. But they kept cutting their losses with cash for corpses sent to the rendering plants.

Trusting British beef farmers bought hi-protein certain-death feed for their cows for the next 18 years. Because the UK had a much higher percentage of sheep than they had cows, every cow got a daily, heaping serving of kibbled sheep. And poor, trusting Brits ate a lot of the infected sheep too. The British like mutton as well as beef. For the first time outside of New Guinea, humans began contracting prions on an ever-increasing amount in their brains.

It should be understood that neither farmers nor butchers fully recognized the problem. At beef slaughter time, the dementia generally had not fully manifested itself. The prions were in the animals, but they had not lived long enough to show the symptoms.

Even if they had, it was not until 1974 that the top UK microbiologist/researcher, Dr. Richard Lacey, and his U.S. counterpart, Dr. Stanley Prusiner, set up their electron microscopes to study prion diseases. Until they did that, researchers thought prion diseases were merely genetic in nature, just weird malformations which occurred from time to time in nature.

The truth is that the damaged proteins (the prions) were not only injuring the bodies of the sick animals, but were passing into the chromosomes—and becoming part of the DNA of those animals and their descendants.

It should be kept in mind that part of the problem is that animals are generally sent to the slaughterhouse before the symptoms of mad cow disease show themselves. But the animal can still have mad cow, especially since he was raised on a ration consisting of dead mad cows and sheep.


BSE (the animal form of mad cow disease) has been epidemic in British cattle since the late 1980s. The first confirmed cases were reported in late 1986; but it is believed that the first case may have occurred in the county of Hampshire in 1985.

In 1985, British farmers noticed that an illness suspiciously like scrapie turned up in a cow. It was a Holstein dairy cow who started kicking, developed an extreme case of the jitters, then fell over dead. Her brain was examined posthumously, its Swiss cheese appearance noted, and the disease given the name "bovine spongiform encephalopathy" or BSE. For the first time, the disease in animals had been named.

In a cow, the bug caused more than just an itch to scrape against fences. BSE was a true "Dementia" disease, like Alzheimer’s is for humans, i.e. memory loss, motor function changes, loss of large movements like walking ability. Eyesight and the ability to make fine movements with the hands were lost, as well as spacial perceptions needed for parking a car, etc. A lot of that is not crucial to a cow, but it was hard for the farmer to milk Bessie when she was splayed on the ground shaking and mooing.

A cow is a lot more valuable than a sheep. So beef farmers demanded answers. At first, nobody connected spastic cows with the scrapie sheep of the 1970s and certainly not with New Guinea cannibals of the 1950s. But in 1986, a research professor of microbiology at Leeds University, consultant to the World Health Organization (WHO), Dr. Richard W. Lacey, announced that scrapie, BSE, and CJD were the same thing; and that this beef disease was in the meat supply. In addition, he not only said it could kill humans, but he warned that a wave of deaths would soon hit Britain.

Immediately, the Establishment set to work to destroy Lacey’s conclusions, and even his character. He was said to be a shoddy researcher and opposed to the best interests of the British people. One publication called him "an airy-fairy, politically suspect vegan." Another said he was trying to dismantle the 6-billion-dollar-a-year British beef industry.

The funding for Lacey’s research was canceled. But, refusing to give up, he warned that there would eventually be a fatal outbreak that would kill many Britons. In a nation whose economy was heavily keyed to beef production and its overseas export, he said people should stop eating beef and the newspapers should start warning people of the possibility of human infection. Lacey went still further and said that 100,000 people in Britain were already infected.

Something had to be done. Beef eaters were becoming worried and beef farmers were frightened. Three things were done to solve the problem. First, Dr. Lacey was fired from his research position at Leeds University. Second, the government established an Official Advisory Council. Of course, they left Lacey, the nation’s only expert, off the board.

Third, the government told the farmers not to worry, that while feeding powdered sheep corpses to live cows probably wasn’t a good idea, Brit farmers could do as they wanted. After all, had not the idea been given to them by American ranchers who regularly practiced "the grisly, fleshly humus pile" method for buffing up beef for huge profits.

The year was 1986. Brits happily went back to eating their cannibal-cattle burgers and steaks, and the beef farmers went back to their rewarding task of supplying them with scrapie-fattened cows to munch on.

Meanwhile, Richard Lacey set to work writing a book on the subject. It was with difficulty that he was able to continue his research; but fortunately, he already had a lot of data in hand. Some friendly researchers also provided secret help. We will discuss the findings of his book in more detail later in this report.


In late 1987, 700 BSE-infected cows were reported in Britain. By the summer of 1988, the number had climbed to 7,000. Out of one side of their mouth, the experts said they were stumped. Out of the other side, they quietly passed a 1988 law, making the use of sheep and bovine offal illegal. ("Offal" is the waste parts of an animal. It includes the intestines, manure residues, and diseased organs.)

But when Europe, Asia, and America heard about this law, they realized the livestock they had been importing from Britain was infected. Immediately they boycotted British mutton and beef, causing millions of pounds sterling profits to vaporize.

Unfortunately, this was a case of too little too late. British livestock were already grazing in every country of the world, and had entered the breeding stock of nearly every nation on the globe. The entire world had been eating imported British beef and lamb chops ever since the disease was solidly in place in the 1970s.

The world ban on beef and the 1988 law against grinding up sheep did not stop the progression of BSE in England. Cows kept dying. The number of infected dead cows soared from 1988’s mere 7,000 to 36,000 in 1992. In eleven years, 160,000 British cows had gone four hoofs to the sky and there still was not an official murmur about human contagion—aside from Crazy Lacey whom no one took seriously.

As already mentioned, the first confirmed cases of the bovine form of the disease (BSE) were reported in late 1986; but it is believed that the first case may have occurred in Hampshire in 1985.

By late 1994, the disease had been identified in nearly 150,000 animals and in just over half of all the cattle herds in Britain. Some scientists (including Lacey) have since stated that the only way to tackle the problem would be to destroy all herds which had cattle incubating the disease. The problem is that the ground would continue to have prions in it.

By the 1990s, news of the deaths from the human form of the disease, CJD (Creutzfeldt-Jakob disease), began to enter the public press. More on that later.