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dilate; it hangs its head; its movements become aimless and its legs, stiff and unbending. Then it starts to grind its teeth; its lips start to twitch, which soon spreads to the muscles around the shoulders and thighs. If suddenly startled, the animal may fall into an epileptic fit. Then the intense itching begins. Finally, the animal becomes completely uncoordinated, paralysis sets it, and it dies. 15 A postmortem will reveal characteristic spongy, hole-riddled areas of brain where the infectious agent has destroyed cells. This spongelike quality gives rise to the name "spongiform," which scientists use to describe this kind of distinctive pathological feature.
So here we have an incurable disease, caused by a mystery "infectious agent," capable of great devastation of sheep flocks, strongly implicated in the development of Mad Cow Disease, and very similar to certain dementia-producing diseases in humans. And we don't know how many sheep are carrying it.
As the British Veterinary Association mildly put it to the House of Commons in a memorandum: "We can only guess at the incidence of the disease. That has been an omission." 16
Actually, successive governments cannot share all the blame for this state of affairs. As one expert, Dr. K. L. Morgan of Bristol University, explains: "The potentially disastrous economic effect of its identification in flocks producing pedigree and breeding stock has resulted in a reticence to acknowledge the presence of Scrapie. The concealment of clinical cases is such that once the first case is diagnosed and the signs recognised, other cases may be disposed of without the knowledge of the attending veterinarian." 17
Scrapie is bad news for everyone. And like all bad news, no one wants to know about it. Until it's too late.
A BIG, BAD BUG
What actually causes scrapie? If you look it up in a medical or veterinary dictionary, you may find it described as a "slow virus" disease. That definition is inaccurate. Scrapie is not caused by anything remotely similar to other recognized viruses. Yet for decades, scientists were happy to classify it as a viral disease for the simple reason that it was inconceivable that it could be anything else. As recently as
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1989, the Academic American Encyclopedia wrote: "Slow viruses are disease agents not yet identified but assumed to exists because the diseases resemble virus diseases in their epidemiology" (my emphasis).
But the scrapie "virus" has never behaved like a virus should behave. No viral particles could be identified from infected tissues. No viral antibodies could be recovered in the laboratory. 18 The scrapie "virus" also violated one of the three golden rules of biology known as "Koch's Postulates," which were established a century ago by the German physician Robert Koch. Koch's third postulate states that, in order to prove that a given infection is caused by particular agent, the agent must not only be isolated from the patient but must also then be capable of being grown in a culture.
But that's not all. Sinisterly, the scrapie resisted the most prodigious efforts to kill it, such as being bombarded with radiation, being cooked at high temperatures, and being doused with strong disinfectant chemicals. None of these lethal assaults could kill the thing that causes scrapie. As one expert commented with justified exasperation: "The fourth decade of my association with Scrapie ended in 1978, with the causal agent still obscure, and virologists as adamant as ever that theirs was the only worthwhile point of view. To explain findings that did not fit in with a virus hypothesis, they re-christened the causal agent an 'unconventional virus.' Use of this ingenious cover-up for uncertainty made 'virus' meaningless—for is not a cottage an unconventional castle?" 19
THREAD TWO: THE LAUGHING DEATH
The place is Papua New Guinea, mostly unexplored by Westerners until the second half of the twentieth century. Before then, nothing but the occasional gold prospector, the odd missionary, motivated by greed or creed, had risked death by malaria to penetrate its secret interior. And there were rumors of cannibalism among the indigenous population.
It is in the distant interior of this island where the Fore tribe make their home. The Lutherans were the first to reach them, in 1949, and the Australians followed two years later with a patrol outpost at a place they called Okapa. The temperature here in the hills is a com-
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fortable 68 degrees F. all the year round, although the humidity can sometimes be disagreeable for a Westerner. The hills and the valleys, once extensively wooded, are now a mixture of trees and grasslands, the result of 11,000 years of continuous human habitation. It may not be paradise, but on first inspection it seems pretty close.
And how deceptive appearances can be. If you had journeyed here some thirty years ago, you would have noticed men, but mostly women, standing and sitting in a distinctive way, their feet spread wide to give them a broad base, a stout wooden pole or spade tightly grasped between both hands, planted firmly in front of them, never relaxing their grip. They sit and stand like this because they must. Without a physical support, they will simply keel over, like an uprooted tree. You see, their spongy brains can no longer be trusted to keep them upright.
These people are dying, and what is killing them is remarkably similar to the "infectious agent" that causes scrapie in sheep.
THE TRUE MEAT OF WOMEN
The Fore tribe cannot be described as living in a state of natural bliss. Sadly, this is no Garden of Eden, if we discount, for a moment, the scrapielike disease that killed up to 80 percent of all women in some villages, 20 we find a society that has several strikingly miserable parallels with our own.
Overpopulation has rarely been a significant problem here, because of frequent tribal wars. In addition, a taboo against copulation while the tribe was engaged in warfare ensured that the birth rate was often low or declining. But the really evident similarity between us and the Fore is the universal malevolence among males toward their womenfolk.
Fore males live together in houses that are strictly segregated from the women and children. Male children are taught from an early age to be disdainful toward females. Adolescent boys periodically go into seclusion to cleanse themselves from the polluting effects that their mothers and sisters radiate. Because the act of copulation is perceived as being fraught with danger, only a married man risks indulgence, for he alone has the power to ward off the evil consequences of such inti-
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mate female contact. Worst of all is male contact with menstrual blood, which may sicken a man, cause vomiting, turn his blood black, corrupt his vital juices, cause his flesh to waste away, dull his wits, and so precipitate his death. 21
If you've ever been tempted to believe in the myth of the "noble savage," the Fore people will bring you down to earth with a bump. It is this deep-rooted hatred of Fore women that, anthropologists believe, led to the outbreak of "kuru"—as this form of scrapie was called. Cannibalism—in particular, the eating of human brains— appears to have surfaced in the Fore tribe for two main reasons: First, the threat of population decline may have resulted in an association being made between cannibalism and increased fertility. Therefore, the more human flesh a woman consumed, the more likely she would be to give birth again, and so replenish the population stock that the belligerent males had thoughtlessly decimated.
And second, as the forests and their animal populations disappeared and hunting became less and less successful, there was a corresponding increase in the domestication of pigs, and the consumption of pig flesh—but only by males. The women, on the other hand, were strongly discouraged from eating highly prized pig flesh, and they therefore resorted to flesh of an altogether different type, which the men would never seek to expropriate. This is why, among Fore males, the human corpse is disparagingly referred to as "the true meat of women." 22
THE UNNATURAL HISTORY OF KURU
"I break the bones of your legs, I break the bones of your feet, I break the bones of your arms, I break the bones of your hands, and finally I make you die." 23
This is the curse which, the Fore believe, when recited by a sorcerer with appropriate gestures and artifacts, will inflict kuru upon his enemy. As a clinical analysis of the course of the disease, it demonstrates an intimate knowledge of its progressively degenerative nature, starting first with increasing difficulty in maintaining balance ("I break the bones of your legs—") and resulting in complete incapacitation ("I break the bones of your hand") before death intervenes.
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The first Westerners to encounter kuru were mystified, and made copious clinical records and case studies. Very often, the earliest dreaded sign of the impending tragedy would not even be noticed by the sufferer herself; a friend or family member would remark upon her shaky balance while crossing a narrow log bridge or climbing over a palisade fence that separates agricultural plots. This stage may last for six to twelve months, during which time the woman's general physical and mental health gradually deteriorates. Eventually, it becomes obvious that walking is difficult and clumsy; the rhythmic and confident swing of her plaited bark skirt is replaced by an unsteady swaying. As the disease progresses, something called the "kuru tremor" takes hold, a rapidly repeating contraction of opposing muscles resembling shivering, sometimes of the whole body, sometimes just the muscles of the face—hence the label "the laughing death." Twitching and shaking make it all but impossible to speak, and she becomes effectively mute. At this stage even sitting upright becomes impossible, and friends may drive a stake into the ground in front of her to grasp, or suspend a rope from the ceiling of her hut so that she may pull herself upright with it. Soon, paralysis and incontinence set in, food cannot be swallowed, and death comes as a sweet release.
Because of its occurrence within families, and its predilection for women, it was first thought that kuru was an inherited genetic disease. However, clever scientific detective work proved beyond doubt that kuru was clearly infectious. How kuru first arose among the Fore tribe is an unanswerable question. What is certain, however, is that the disease was transmitted by eating meat—in this case, human meat.
Yet even at the height of the devastating kuru epidemic, the proportion of people infected with the disease in the population was iive times less than the calculated incidence of Mad Cow Disease in the British adult cow population. 24 That tells you something about the breathtaking dimension of the plague among our animals.
Of course, it would be easy to dismiss kuru as an isolated, freak disease, of no possible consequence to anyone in the modern world, if it were not for one fact: We in the West also have our own form of kuru.
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THREAD THREE: BRAIN DEATH
There is a disease that is so feared by some members of the medical profession, that pathologists have refused to perform autopsies on patients who are suspected of dying from it. Operating room technicians have refused to be present when these patients are operated on; recently, the director of a pathology laboratory was so worried about the possible risk of contagion that he ordered the destruction of histology slides taken from infected patients. Astonishingly, some hospitals have even refused to admit patients suffering from it. 25
What possible disease could cause so much terror among doctors? It is, of course, a disease caused by that familiar "infectious agent"— an "agent" that cannot be destroyed by boiling, is immune to ultraviolet and ionizing radiation, resists most common forms of disinfectants, and can survive for long periods in apparently hostile conditions. Tissue samples taken from humans, fixed in formalin (a powerful disinfectant and preservative), and then embedded in paraffin have still been found to be capable of causing fatal infection. 26
The name of this dreadful affliction is Creutzfeldt-Jakob disease. "Creutzfeldt" (pronounced "kroytz-felled") after the scientist who diagnosed the first case in a twenty-two-year-old woman in 1920; "Jakob" (pronounced "yack-ob") after the physician who diagnosed the next three cases in the following year. It is often abbreviated to just its initials, CJD.
The disease shares many familiar symptoms with those already described. The time between infection and commencement of the first symptom can be very long indeed—up to thirty-five years has been recorded. 27 On the other hand, in cases where infected material has been placed in direct contact with a patient's exposed brain (for example, during brain surgery with contaminated instruments), the disease can manifest itself within two years.
Forgetful periods are common at first. Poor concentration, difficulty in finding the right words, depression, inexplicable feelings of fear, and aggressiveness are all frequent initial symptoms. Patients complain that objects look "strange," attacks of vertigo and dizziness occur, and so does ringing in the ears. There is widespread tingling or numbness. It becomes more difficult to walk, an effort to climb stairs,
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fine movements such as writing or sewing become difficult or impossible. The patient may fall down while turning around. And all this is simply the first stage of the disease.
The second stage is characterized by a lack of control over bodily movements. Trembling, writhing, and uncontrollable jerking spasms occur. At the same time, the body, or parts of it, may become very rigid. Visual disturbances and hallucinations occur.
The final stage of CJD consists of an appalling decline into a vegetative state. Patients become mute and unresponsive, incontinent, and unable to feed. In medical language, they appear "decerebrate"—as if the brain stem has been cut to eliminate brain function.
You can see why some health workers are so fearful of this terrifying and incurable disease.
TYING THE THREADS TOGETHER
So there we have it: an unholy trinity of three very closely related diseases, two of them present in humans, one in sheep; all fatal and all caused by an unknown agent that challenges the most basic concepts of modern biology. After all, just how can a disease be transmitted from one person to another without the help of DNA or RNA (chemical substances involved in the manufacture of proteins and essential to the genetic transmission of characteristics from parent to offspring)? "It's the stuff that Nobel prizes are made of," says Charles Weissmann, a leading researcher in infectious brain diseases. 28
For decades, however, there was comparatively little mainstream scientific interest in this baffling group of diseases. That which cannot be smoothly explained is all too often ignored, even by scientists who should know better. And there was no overriding urgency to the problem: The incidence of Creutzfeldt-Jakob disease in the population was considered to be very low, kuru had been slowly dying out ever since cannibalism had been outlawed among the Fore tribe, and scrapie, well, scrapie had always been with us. Why should increasingly hard-pressed scientific resources be allocated to this peripheral area of interest? A strict cost-benefit analysis, much beloved by those officials who control today's science, would not justify the investment.
In November 1986, all that changed forever. In that month, brain
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tissues sent to Britain's Central Veterinary Laboratory, by puzzled veterinary surgeons, were scrutinized by experienced neuropathologists. Under the microscope, the distinctive hole-riddled areas of brain could be clearly distinguished and photographed. They had seen it before, of course, in specimens taken from diseased sheep. But this was something very new indeed—the samples under the microscope weren't from sheep, they were from cows.
Something rather strange seemed to have happened. Scrapie, present in the sheep population for hundreds of years, appeared to have crossed the species barrier and had mysteriously infected cows. Suddenly, decades of work by a few dedicated scientists on kuru, Creutzfeldt-Jakob disease, and scrapie acquired a new and urgent relevance. Because, as Dr. Tony Andrews, a senior lecturer at the Royal Veterinary College, put it: "Now we know that Scrapie has jumped from sheep to cattle there is nothing to suggest it may not, in future, wind up in people." 29
JUMPING THE SPECIES BARRIER
It has been known for decades that scrapie, kuru and Creutzfeldt-Jakob disease are all extremely similar—so similar, in fact, that scientists term them all "spongiform encephalopathies." Encephalopathy is a word used to describe any degenerative illness of the brain: in this case, one that causes parts of the brain to resemble a sponge riddled with holes.
It has also been established beyond any doubt that many spongiform encephalopathies possess the ability to cross the species barrier. For example, if you take tissue from a human suffering from Creutzfeldt-Jakob disease and infect goats with it, they will die from scrapie. 30 Now consider this evidence:
• The agent that causes Creutzfeldt-Jakob disease in humans has been experimentally inoculated into chimpanzees, capuchin monkeys, marmosets, spider monkeys, squirrel monkeys, woolly monkeys, managabey monkeys, pig-tailed monkeys, African green monkeys, baboons, bush babies, patas monkeys, talapoin monkeys, goats, cats, mice, hamsters,
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gerbils, and guinea pigs. Subsequently, all these animals succumbed to spongiform encephalopathy.
• The agent that causes scrapie in sheep has been experimentally inoculated into mink, spider monkeys, squirrel monkeys, cynomolgus monkeys, goats, mice, rats, hamsters, and voles. Subsequently, all these animals succumbed to spongiform encephalopathy.
• The agent that causes kuru in humans has been experimentally inoculated into chimpanzees, gibbons, capuchin monkeys, marmosets, spider monkeys, squirrel monkeys, woolly monkeys, rhesus monkeys, pig-tailed monkeys, and bonnet monkeys. Subsequently, all these animals succumbed to spongiform encephalopathy. 31
I want to make it clear that I don't approve of experiments such as these. They are often needlessly repetitive and horribly cruel for the poor animals concerned. The traditional justification for vivisection is that it advances human knowledge, but in the case of these experiments, that excuse is less valid than ever. Because in the public debate that arose after Mad Cow Disease—later known as bovine spongiform encephalopathy (BSE)—was diagnosed, officials went to great pains to stress the extreme implausibility of BSE being passed from cows to human beings, even though they must have known that scientific findings such as those above proved nothing of the sort.
Concealing the truth about spongiform encephalopathy was nothing new for British officials, however. They'd done it before.
A BREACH OF TRUST
In the United Kingdom during the period 1959 to 1985, several thousand children were injected with human growth hormone, a treatment for dwarfism. At that time, human growth hormone was extracted from pituitary glands removed from the brains of corpses. A considerable number was needed, about 100 glands to treat one child per year, and in order to achieve this quantity, mortuary technicians were offered a cash incentive.
"We were given 10 pence (about 14 cents) per pituitary," said one
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technician, "and you never sent away less than twenty or in some cases forty depending on how quickly you could gather them." While some technicians were careful not to take glands from patients who had died from infectious or dementing diseases, others were not so painstaking. "All they were interested in was the cheque when it came in," said the same technician. "The more you sent off, the more money came in. You could pick up twenty-five to thirty pituitaries and not argue about it, just take the whole lot and send them off, and that was £3 (about $4.25)." 32
During the course of research for this book, I interviewed Dr. Helen Grant, one of Britain's most experienced neuropathologists. She explained to me in graphic terms what would happen: "I was one of the pathologists who did postmortems in those days," she told me. "And I remember when I was about to drop the pituitary I had just removed into formalin, the mortuary technician would say, 'Just a minute doctor, do you want that pituitary?' And I would say, 'No, I don't think I do, why?' 'Oh well, can I have it?' he would ask. 'You can have it,' I'd say, 'but what are you going to do with it?' 'Well,' he'd reply, 'we've got to collect them for research.' Well of course I'd let him have it. It was for 'research,' you see. Never for one instant did I suppose that it was going to finish up being used in a therapeutic way—being used as a treatment on children. As far as I knew, these pituitaries were going for research, and research only."
Because the supervising authorities failed to implement sufficiently stringent procedures for the collection of pituitary glands, an unknown number of children became infected with Creutzfeldt-Jakob disease. To date, seven patients who were given growth hormone have died from CJD. 33 Not all recipients of human growth hormone treatment were (or will be) affected and no recipients of the treatment after autumn 1985 are at risk (the time when the manufacturing process of human growth hormone changed; an entirely pure form is now genetically engineered from the bacterium Escherichia coli).
But now comes the most outrageous part of this sad history. When evidence of the disaster began to emerge, the British Department of Health decided not to tell the patients that their lives might have been put at risk. They decided that to inform the patients who might have been injected with Creutzfeldt-Jakob disease would only cause panic.
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So there was no public enquiry into this unfolding tragedy. . . . Just silence.
In the United States, the patients and families affected were notified as soon as the full significance of the situation was recognized. But not in Britain. Dr. Grant explains: "There was pressure to inform the families at the time the problem was first recognised. But it was decided not to. Why did they sit on it for seven years? Why did they sit on it at all? I suppose because it looks bad. And the effect of it was, you see, that some of those children may later have become blood donors. How about that?"
In justification of its policy of secrecy, the Department of Health stated, "The right to know was balanced against the anxiety that would be caused to these patients about a condition which is invariably fatal." 34 A blood-curdling statement indeed, and one that makes you wonder what other unpleasant facts have been concealed from us in an attempt to protect us from "anxiety."
After mounting pressure, it was eventually conceded in late 1991 that recipients of the injections should, after all, be contacted and informed of the risks. And what of compensation? There simply are not words to describe the profound personal suffering involved in this dreadful business. Surely, there is no possible excuse, and no honorable pretext, for not generously compensating both patients and their families?
"Any legal action would be defended on the grounds that as regards clinical factors at the time it was administered the treatment conformed with knowledge then available about good clinical practice," said the department in a statement to journalists working on a television program. 35
"WE THOUGHT WE WERE SAFE, BUT WE WERE WRONG"
In the 1970s, the British Medical Research Council wanted to ensure the safety of the procedure for extracting human growth hormone from the pituitary glands of corpses. Professor Ivor Mills, professor emeritus of medicine at Cambridge University, was a member of the Endocrine Committee, whose task it was to advise on safety.
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"I was on the Endocrine Committee of the Medical Research Council in the 1970s," said Professor Mills, "when we had to consider whether it was safe to extract human growth hormone from human pituitaries, because you know the pituitary is attached to the brain and it seemed to us that there might be some possibility that Creutzfeldt-Jakob disease would be in a form that was in the pituitary and we might transfer that to the children who had to be injected with growth hormone. We took advice from many experts, including Scrapie experts, because we thought there might be some relationship between the two diseases and we were advised at that time the technique was safe. We have since been proved to have been wrong and I feel rather guilty myself that this happened and two children in this country, and rather more in the rest of the world, have been inflicted with dementing fatal illness. I am anxious since there is a relationship between Creutzfeldt-Jakob disease, I think, and Scrapie that the same sort of mistake should not be made a second time because, as Professor Southwood pointed out, the results could be very serious indeed." 36
As a result of the human growth hormone tragedy, Professor Mills became so concerned that the mistakes of the past should not be repeated that he personally testified in front of the British parliamentary committee inquiring into BSE. His evidence makes arresting reading, due in part to his distinguished scientific credentials, and in part to his obvious depth of concern. In a memorandum to the parliamentary committee, Professor Mills described how the experts at the time of the human growth hormone disaster had judged the procedure to be safe.
"We took advice from several experts including Scrapie experts and thought the technique was safe. Yet two children in this country got Creutzfeldt-Jakob disease. It is now known that this disease is very similar to Scrapie.
"We thought we were safe but we were wrong. We have made a mistake once and as a result two children got a fatal disease. We cannot afford to make the same sort of mistake again because the result would be much more disastrous. We now know much more about the agent which causes Scrapie and CJD and similar neurological diseases in man. The agent is unique and, in my opinion, highly dangerous to spread widely." 37
In his evidence, Professor Mills made four important recommen-
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dations. First, and most important, he wanted to prevent potentially infected material (lymphoid tissue, brains, and spinal cords from cows, sheep, and goats) from being fed back to food animals. Second, he wanted to see controls extended to include calves of six months and younger. Third, he wanted to make sure that potentially infected material was not allowed to contaminate other meat in the slaughterhouse or anywhere else, and last, he proposed that calves born to cows known to be infected with BSE should not be used for breeding.
All eminently sensible precautions, in view of the devastating and enigmatic nature of the infectious agent. The human growth hormone tragedy had already proved that even the country's top experts could be terribly wrong about this disease. As Professor Mills had written previously in a letter to The Times: "What I think we should learn from this is that it is not good enough to say the chances of harm, we think, are very small." 38
That is a sensible, cautious attitude, based on hard-learned experience. But it was not the position of the British government, which constantly sought to reassure the public that there was no risk. As John Gummer, the minister for agriculture bluntly put it when testifying before the parliamentary committee: "The plain fact is that there is no evidence that BSE poses any risk." 39
That, of course, was a politician's statement.
A JOURNAL OF THE PLAGUE YEARS
No evidence? Here is the chronology of BSE. Read it, and make up your own mind.
On December 13, 1985, a portentous report appeared in the British press that, with hindsight, could be considered a curtain-raiser to the whole BSE saga. "It's Dog Eat Dog on Swedish Farms," exclaimed the headline. 40 "Many of the Christmas hams now on sale here have come from pigs fed on the minced carcasses of sick animals," wrote a journalist from Stockholm. The story had particularly revolting aspects. For several years, the rotten carcasses of diseased cows and pigs, as well as formerly loved pets, had been covertly processed to make food for cows, pigs, poultry, and domestic pets. Dairy farmers began to
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suspect the wholesomeness of their animals' feedstuff when their cows started to fall ill and decrease milk production. Despite attempts to conceal the size of the scandal, news eventually reached Swedish consumers, who were predictably outraged that their pets were being recycled with quite so much ruthless efficiency. With great prescience, the report also queried the wisdom of turning "the traditionally vegetarian cow" into a carnivore, not to say a cannibal.
For the average British reader, it was a relatively trivial story. What the Swedes were up to on their own farms was their own business. And in any case, it couldn't happen here, could it? There were probably laws to prevent that sort of thing. Yes, indeed. Ignorance could be so blissfully comforting.
By the time this report appeared, the first cows were already dying from BSE on British farms. But as yet, very few people realized what was happening.
Nine months later, another strangely prophetic article appeared in the science pages of a British newspaper. 41 Headlined "The Disease That Bugs Biochemists and Sheep," it described how the "exotic, utterly mysterious agent" that causes scrapie mystified scientists. How could a lethally infectious agent exist that possessed neither DNA nor RNA? "Future work in this field is sure to be immensely interesting," the piece enthusiastically concluded, with massive understatement. Quite so.
THE RENDERERS SURRENDER
Meanwhile, dire things had been happening to an obscure part of Britain's meat industry. Rendering is a little-known but essential element of the strange economic equation that holds together all the diverse sections of the flesh trade. Renderers take all the bits and pieces of animals from slaughterhouses that no one else wants, boil them up, and produce fat and protein. The fat is then turned into products such as margarine and soap, and the protein makes animal feed. Thus, they serve two essential functions: they act as a garbage disposal service for one and a half million tons of mangled corpses every year, and they act as a cheap source of feedstuff for the next generation of food animals, which in due course are fed to the follow-
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ing generation, and so on. As the chairman of their trade association put it, "If there is no rendering industry, there is no meat industry." 42
No one really seems to have considered whether it was such a good idea to force naturally vegetarian animals such as cows to become carnivores and cannibals. It made sound economic sense; so they did it. But as former British Minister of Health Dr. Sir Gerard Vaughan explains, when you monkey around with nature, it is wise to expect some nasty surprises: "One of the main areas of fault is the processing of animal food using parts of the same animals. It's not a natural instinct for one animal to eat its own species, in fact it's totally foreign to it. That seems to be nature's understanding of the bacteriological and biological dangers, because if one animal starts to eat its own stock, then the dangers of infection increasing are very great indeed." 43
By the middle of the 1980s many Tenderers were themselves close to the brink of extinction. The low price of vegetable oil on the world markets had made the Tenderers' own animal fat product uncompetitive, and the drive toward healthier eating had made edible animal fats increasingly unpopular among food manufacturers. Denied income from this vital market, the economic equation just wouldn't hang together any more. In 1986 alone, 10 percent of the industry went bankrupt. 44 The industry appealed to the government for help, but in vain. Then they tried charging slaughterhouses a fee for the disposal of animal waste, to the considerable ire of the slaughterhouses, some of whom illegally took waste disposal into their own hands. "I know of abattoirs in the North West of England and the Midlands," the then-chairman of their trade association was quoted as saying, "that minced up offal and started spreading it on fields rather than pay for it to be disposed of by Tenderers." 45
Survival in a harsh economic climate is largely a question of efficiency, and the rendering industry had already started to take steps to modernize its methods and reduce its costs. The old procedure for rendering animal flesh and bone was a two-stage operation: first, the foul brew would be cooked up in a huge vessel and the fat separated from the solid (known as "greaves"), then, the greaves would be further processed, often with a solvent such as benzene or petroleum spirit, to draw off more fat, and finally leave a meat and bone meal product.
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The new procedure differed in several ways: it was a continuous process, not a batch system, and the use of solvents to extract fat was discontinued in favor of mechanical pressing and centrifuging. It would later be speculated that these changes in the rendering process were the root cause of the BSE epidemic.
PUTTING THE LID ON
Sources indicate that another case of BSE was seen in January 1986, and this triggered the involvement of the government's own veterinary experts. We shall never know precisely when BSE was recognized as a scrapie-like disease, although the chief veterinary officer for the Ministry of Agriculture said on television that it was diagnosed "within a few weeks." 46 The visible effects of spongiform encephalopathies are quite distinctive—no other disease leaves such a dramatic, hole-riddled brain as evidence of its infection. And the government's veterinary experts would certainly have seen this type of disease in sheep, under the name of "scrapie." Now, the key question is, why did it take so long—over two years—for the government to begin to take any effective action? After all, here we have an entirely new disease of cattle, very similar to the lethal and incurable scrapie in sheep. If a disease of this severity and lethality suddenly starts crossing the species barrier, shouldn't that be taken as an extremely disquieting development? Surely, the alarm bells should have started ringing as soon as those government experts saw the warning signs?
Well, perhaps they did. Neuropathologist and fellow of the Royal College of Physicians Dr. Helen Grant believes that there was a policy of official silence on the matter. And since she has spoken to many of the key scientists involved, she ought to know. She told me:
"A lid was put on it. As soon as they figured out what the disease was likely to be due to, they should have stopped feeding cattle with contaminated feedstuff. But the government didn't. They let it go on, until the Southwood committee finally stopped it."
Professor Richard Lacey agrees. Much reviled in official circles ("he seemed to lose touch completely with the real world," sniffed the 1990 parliamentary inquiry into BSE 47 ), Professor Lacey was one of the most outspoken critics of government policy during this period.
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And his views could not lightly be dismissed: as a clinical microbiologist with a worldwide reputation, and a fellow of the Royal Society of Pathologists, he was well placed to comment. Professor Lacey believes that money was at the root of official inaction:
"The available evidence suggests," he wrote, "that there has been a carefully orchestrated manipulation of public opinion by the Government in order to avoid taking action. The main reason for this is the sheer scale of the action that would be needed. The cost of compensation for replacing say six million infected cattle could run into billions of pounds. Moreover, the adverse international publicity this would generate might effectively put the UK into quarantine with loss of food exports, tourism, and even a substantial part of our industrial base." 48
THE STORY BREAKS
In November 1986, the official record shows that the government's Central Veterinary Laboratory formally identified bovine spongiform encephalopathy, but ministers within the government were not informed until June the following year. 49 And even then, it took ten more months—until April 1988—for the government to decide to appoint a committee to look into the disease (known as the South-wood committee). Why all these delays?
Again, we can only speculate about the real reasons. The official justification is that "transmission experiments" were needed, in which infected tissue from cows would be injected into mice. You might think that it was already painfully established that the new disease had almost certainly been transmitted—from sheep to cows. More cynical observers might conclude that, in reality, a gamble was being taken that the outbreak was small and containable, and that it could be quietly dealt with before it blew up into a major "food scare." If this was the case, the bet failed miserably.
In October 1987, BSE finally went public—but in a very demure and modest way. A brief paper, barely covering two sides, appeared in the professional journal The Veterinary Record in the section entitled "Short Communications," just above an advertisement for magazine
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binders. 50 It described the disease in clinical terms, showed some photographs of diseased brains, and proposed the official name for the disease: bovine spongiform encephalopathy. The paper concluded with a careful warning—despite BSE's striking similarity to other spongiform encephalopathies (such as scrapie and Creutzfeldt-Jakob disease) its cause was unknown, and "no connection with encephalopathies in other species has been established."
The response of other media was appropriately low-key, most treating it as something of a scientific oddity. "There have been suggestions," wrote the agriculture correspondent of The Times, a couple of months later, "that it could be linked to a sheep disease called Scrapie," but the short article concluded by quoting another expert as not yet seeing BSE as a serious threat to cattle health. 51
By April 1988, it must have become excruciatingly obvious to those in authority that BSE was not going to go away peacefully. By now, over 400 cases had been reported in Britain, even though the disease was still not officially notifiable. Clearly, the world was on the verge of an epidemic of unknown magnitude, and something had to be done. The shrewd political response to this sort of tricky situation is to appoint a committee. Committees give politicians breathing space: their advice is not binding, and they provide an effective shield with which to deflect criticism. And that is what the government did—on April 21, the Southwood committee was announced to the world. "A working party headed by Sir Richard Southwood, professor of zoology at Oxford, has been set up by the Ministry of Agriculture and the Department of Health," reported the Sunday Telegraph, "after complaints from vets that the Government has been dragging its feet." 52 Sir Richard had the advantage of also being chairman of the National Radiological Protection Board, and was therefore accustomed to a high-profile, controversial position. Tagged onto the official announcement was some typical public relations baloney. "The Ministry of Agriculture said there was no evidence of the disease being transmitted between animals and no evidence of it being passed on to people through meat and milk," the newspaper reported.
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THE SUBTLE ART OF DECEPTION
The propaganda battle had now begun in earnest. At stake was a market for beef and veal worth about $3 billion and, as in all battles, truth became the first casualty. It became impossible, for example, to establish just how hard the market for beef had been knocked.
At the worst of the crisis, the head of Britain's largest chain of retail butchers was quoted in their trade journal as saying there had been "no reduction" in beef sales. 53 However, the parliamentary committee said the market had dropped by 25 percent, 54 and newspaper reports indicated that it might have plummeted by as much as 45 percent. 55
Official statements began to be peppered with the sort of evasive language normally only used in times of war. Defensive phrases such as "no evidence" and "no proof" recurred time and time again in official proclamations. In particular, the defense of "no evidence" would be used repeatedly to quell rising public concern.
When the Ministry of Agriculture claimed that there was "no evidence of the disease being transmitted between animals" they were, of course, being economical with the truth. The evidence already strongly suggested that there had indeed been "transmission between animals," inasmuch as cows had almost certainly contracted BSE from scrapie in sheep, and extensive experimental work had already established that scrapie could be transmitted to many other mammals.
And as far as transmission between cows was concerned, it was simply too early to make any kind of prediction. As the government's own vets rather embarrassingly pointed out within a few days of the ministry's nonsensical proclamation quoted above, "Until it is known whether or not the cow is an end host, it is not possible to say if the offspring of affected animals will themselves be infected." 56 The two announcements were, of course, directed toward totally different audiences—the government's vets were speaking to other professionals, and the Ministry of Agriculture was addressing the public at large.
Thus do our rulers deceive us.
By now, intelligent people were starting to ask some penetrating questions. A thoughtful paper appeared in the Veterinary Record under the title "Bovine Spongiform Encephalopathy: Time to Take Scrapie Seriously." 57 It was written by K. L. Morgan, a lecturer at
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Bristol University, who pointed out that tissue taken from patients dying from Creutzfeldt-Jakob disease could infect goats with scrapie, and also cause a similar disease in cats. And scrapie could also be transmitted from sheep to monkeys. In addition, it had been experimentally demonstrated that passage through animals could alter the "host range" of the scrapie agent—in other words, if scrapie had jumped from sheep to cattle, it might now become more directly infectious to human beings. This, of course, would be the ultimate "nightmare scenario."
A couple of weeks later, the government's own veterinary service also published an article in the same journal, which included the following memorable passage: "BSE must be seen in perspective. The number of confirmed cases (455) is very small compared with the total cattle population of 13 million. The number of cases is expected to increase but if as is anticipated, it behaves like similar diseases in other species only small numbers of incidents relative to the total number of cattle disease incidents are likely to occur." 58
Did you follow that? The logic is, to say the least, convoluted. What they appeared to be saying was this: "There are currently only 455 cases of BSE, so don't panic. And even if that number increases, it will probably be a small fraction of the total number of sick cows around, so there's still no need to panic." Four years later, we are well on the way to 100,000 cases of BSE, but presumably there are still lots of sick cows who don't have BSE. Apparently, we are supposed to find this reassuring.
BRAIN FOOD
To their credit, the Southwood committee worked quickly, although there was criticism that none of its members were familiar with spongiform diseases. 59 In June 1988, BSE was at last made a notifiable disease, and a six-month ban was imposed (effective from mid-July) on the feeding of "animal protein" to cows and sheep. For six months, at least, these animals were to be allowed to live like vegetarians again—cannibalism was no longer compulsory—although poultry and pigs still continued to be flesh feeders. By August, it was announced that cattle known to be infected with BSE (i.e., already in the terminal stages of
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the disease) were to be slaughtered and their carcasses destroyed. While it was clear that the Southwood committee was spurring the government into some action, it was inexcusable that the full committee's report would not be made public until February 1989.
Furthermore, the action taken was far from adequate. Following an article in a British medical journal, the Times pointed out in June that there was still no legislation to stop manufacturers from adding cows' brains to meat products intended for human consumption, and no requirement for appropriate labeling. 60 "It seems odd," said Dr. Tim Holt of St. James Hospital in London, "that they have banned cattle from eating these cattle brains, but they have not banned humans from eating cattle brains." 61
Odd? Or scandalous?
So here was the position: because the disease could not be detected by any test in the living cow, only those cows who exhibited symptoms—and who were therefore in the last stages of the disease—had to be destroyed. Other cows—and in particular, meat from the most suspect organs—could still enter the food chain.
It was now more than eighteen months since the official identification of the disease by the government's Central Veterinary Laboratory.
WHISTLING IN THE DARK
In August 1988, the Ministry of Agriculture announced that it would pay farmers 50 percent of the market value for cows that had to be slaughtered following infection with BSE. 62 This penny-pinching compromise pleased no one. Farmers were outraged that they were being denied full compensation; consumers were worried that farmers would be tempted to sell infected cows into the food chain rather than destroy them for half their value. About this time, too, concerned voices began to be heard on the subject of scrapie. Dr. Tony Andrews of the Royal Veterinary College, for one, was quoted in a newspaper interview as saying: "There is evidence to suggest a link between scrapie and Creutzfeld-Jacob disease, which causes premature senility in people. There have been experiments where tissue from the brains of dead victims of this disease has been put into goats which then contracted scrapie." 63
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Dr. Andrews wanted the government to introduce an eradication policy for scrapie, starting with the establishment of a register of scrapie-free sheep. The Ministry of Agriculture was characteristically cool about the idea, saying that "in the light of known medical evidence" it could not be justified. An anonymous ministry spokesman then outlined the official line: "Scrapie has been known about for 400 years and there is no evidence that it has ever spread to people."
The Department of Health also got in on the act, echoing the belief that there was "no proof" of a link between scrapie and human diseases. This hypothesis would later be given ministerial weight when John Gummer testified before the parliamentary committee enquiring into BSE.
The ministry's propaganda machine seriously lost credibility a few days later, however, when Dr. James Hope, head of a government-funded but independent research unit studying the disease, seemed to contradict their unctuous reassurances. While agreeing with the government's position that there was "no evidence" that humans could catch the infection from eating beef (indeed, how could there be with such a slow-developing disease?) he went on to say: "Of course there is alarm because it's potentially a great threat to the livestock industry as well as to human health. Because it jumped from sheep to cow, it might better be fitted to jump from cow to human." 64
Yes, indeed it might. And that was a possibility that no amount of official whistling in the dark could exclude.
By now, several countries had decided to ban the import of British cattle. And in October, the results of the government's "transmission experiments" to mice showed that BSE could indeed infect other species—extremely bad news for the public relations blowhards. Then in December, legislation came into force prohibiting the sale of milk from "suspected" cattle, and the ban on recycling animal protein back to cows in their feed was extended for twelve months.
Also in December, scientists from the government's Central Veterinary Laboratory published damning evidence showing that the source of BSE was contaminated cattle feed. 65 "The results of the study," the scientists wrote, "do, however, lead inevitably to the conclusion that cattle have been exposed to a transmissible agent via cattle feed-stuffs." In other words, cows had been eating scrapie-infected sheep.
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PICTURES FROM THE END OF THE WORLD
So began a strangely apocalyptic period in recent British history, dramatically illustrated a decade later by some extraordinary contemporary photographs. As I write, I am looking at some of the most surreal pictures I have ever seen in my life—pictures of the farming folk of Merrie England, busily burning hundreds, eventually thousands, of their own cows.
Here is a photograph that is both ludicrous and chilling: It shows a secret Ministry of Defence location, where cows are being burned. Operatives dressed in nightmarish chemical warfare suits are clambering over earth mounds, digging ditches, maneuvering heavy-duty Army cranes from which dead cows swing. It looks like a science fiction nightmare: doomsday Lilliputians swarming over a herd of upturned bovine Gullivers. The very notion that vast herds of British cows should receive secret military funerals is beyond farce, beyond satire. While some cows go to make meat pies, other cows receive state funerals. For services unrendered, perhaps.
Another widely reproduced photograph of the time starkly conveys the surreal, Gotterdammerung-like quality of it all. It is simply a picture of Armageddon. There they lie, like vanquished warriors, a herd of supine cows, legs splayed, carcasses bloated with gas, while the flames of hell lick around them and ghostly clouds enshroud them. If you were to photograph the end of the world, it would probably look something like this. This was a disturbing, archetypal image that millions of people saw all over Britain's national media; maybe it reminded them of the evil forces that modern agriculture had unleashed on the world, and how very close we all might be to bio-cataclysm.
But perhaps the most widely seen image of all was that of four-year-old Cordelia, daughter of Britain's then minister of agriculture, John Selwyn Gummer. No history of BSE is complete without mention of Cordelia, the little girl who, for a few awkward minutes in 1990, was conscripted into service for the ministry, and posed with daddy before the world's media, cow burger in hand—a spectacle that one seasoned journalist movingly described as a "deeply distressing sight." 66 Today, as politicians increasingly demand that the intrusive
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media leave their personal lives unexamined, and threaten oppressive legislation to enforce their "right to privacy," it is appropriate to remember poor Cordelia.
What possessed the minister of agriculture to involve his little girl in such a public relations exercise is hard to fathom. Perhaps it was intended to reassure us all that, if the minister was willing to expose his own family to British beef, then all must be well. But to many, it must have seemed a cheap and cynical publicity gimmick. This "televisual pantomime"—as the science editor of the Independent newspaper called it—"of the Minister of Agriculture attempting to force feed his daughter with a beefburger" was all too easy to see through. "This is the man," wrote the science editor, "or to be charitable, the successor to the men, who acquiesced in turning cattle into carnivores and chickens into cannibals. And he is surprised that the public does not take his word on food safety." 67
It was also a particularly capricious hostage to fortune. If, in later life, Mr. Gummer's daughter should ever fall ill with any meat-related disease (and I sincerely hope she does not), then you can be sure that those press photographs will reappear to haunt her. In the apt words of Shakespeare: "Upon such sacrifices, my Cordelia, the gods themselves throw incense." 68
AN OFFAL YEAR
Things were looking decidedly bleak for the meat industry, and in 1989 they got even worse. The year started with a lambasting for the government from a very surprising source—Lord Montagu of Beaulieu, one of England's most prominent landowners. One of his tenant farmers reported having a cow with BSE in 1987, which, Lord Montagu learned with astonishment, could legally be sent to market. "I am amazed at the slow reaction of the ministry and the complacent attitude it had at the beginning," stormed his lordship, who also wrote to John MacGregor, then minister of agriculture. With an inevitable turn of phrase, a ministry official once again answered the charge of complacency by repeating the official mantra: "There is no evidence to suggest that BSE can be transmitted to humans through meat." 69
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"They are guessing, and hoping," said Professor Richard Lacey. "They have a public voice which is trying to reassure everyone, but an inner fear. I think they know there's a real problem much worse than they're letting on." 70
"THE IMPLICATIONS WOULD BE EXTREMELY SERIOUS"
Public and professional disquiet was steadily mounting. In early February, the Guardian newspaper ran a front-page report headlined "Meat risks report 'held back,' " which alleged that a report into the risks of BSE to human transmission was being officially expurgated; this was subsequently officially denied. 71
A few days later in the same paper a letter from expert neuropathologist Dr. Helen Grant of London's Charing Cross Hospital was published, which pointed out: "There are no laboratory tests to identify such [BSE-infected] animals: the only way to establish the diagnosis is to examine the brain. Such animals, thought to be healthy, will be slaughtered and enter the food chain . . . there is no doubt that animals harbouring the virus but seeming healthy have finished up as beef." 72
The next day, The Times's medical correspondent, Dr. Thomas Stuttaford, echoed rising medical concern: "Neither Mrs. Thatcher nor her scientific advisers can be sure that these organisms [BSE] . . . have not been already picked up by people as they enjoyed a piece of marrow in an Irish stew, or ate a meat pie which had contained brains or meat from an infected, but not yet stricken, animal." 73
The Southwood report was published at the end of February, and its main conclusion was: "From present evidence, it is likely that cattle will prove to be a 'dead-end host' for the disease agent and most unlikely that BSE will have any implications for human health. Nevertheless, if our assessments of these likelihoods are incorrect, the implications would be extremely serious." 74
Officials responded warmly to the first part of the conclusion. The Southwood committee had also described the risk to humans as "remote," and this now became the official buzzword, largely replacing the "no evidence" slogan used up until then.
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But quite soon, it would be demonstrated that cattle were not, in fact, the "dead-end hosts" the committee had proposed, and that the disease could be further transmitted to other species (cats for example). Nevertheless, the Southwood report would now be used to give additional substance to the assertion that "beef is safe." As Professor Lacey pointed out: "Even after the cat deaths, the only official action seems to be the parrot-like claim from ministers that our beef is completely safe." 75
The key concern now was this: it was known that the "infectious agent" was concentrated in certain organs, notably the brain, spleen and thymus glands. Cattle could be infected with BSE, but not show obvious signs, and there was nothing to stop their organs ending up in the food chain as offal. The Southwood committee had wondered whether meat products containing brain and spleen should be labeled as such, but "did not consider that the risks justified such a measure." 76
However, they did suggest that offal—brain, spinal cord, spleen and intestines—should not be used in the manufacture of baby food—a rather contradictory recommendation, in view of their basic postulate in favor of the safety of beef. 77 In addition, it was announced that the government's chief medical officer advised mothers not to feed infants under eighteen months on this material. 78 This contradiction was spotted by one member of parliament, who promptly asked the Prime Minister (Margaret Thatcher), "If, as appears likely, BSE is a threat to humanity, why not ban it foffal] for all human food—or, if it is not a danger, as it is not according to the Minister of Agriculture, why ban it for babies?" The Prime Minister dodged the question, saying there was no point setting up a committee and then not taking their advice. 79
Estimated Likelihood of a Meat Eater Consuming a BSE Infective Agent
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HOW NOW, MAD COW?
Meanwhile, some startling revelations were coming to light. On March 13, a question was asked in the House of Commons to establish whether the Ministry of Agriculture had commissioned research to find out whether BSE would infect human cells. Donald Thompson, the parliamentary secretary to the Ministry of Agriculture, answered, "No, but trials are under way using marmosets, which are primates." 81
This was a staggering admission. The official line had always been that there was "no evidence" that BSE posed any risk to human health. Well, of course there was "no evidence." If you don't commission the research, you don't have the evidence!
This Alice in Wonderland logic had surfaced in parliament a few days earlier, when Mr. Thompson was asked how frequently the Ministry of Agriculture had tested samples of cattle feed, to check that the ban on cows and sheep in cattle food was actually working. He replied, "Ministry officials are empowered to take and test samples of ruminant feedstuffs if they have reason to believe the ban on the use of ruminant-derived protein is being broken. To date, there has been no reason to believe the law has been broken and such action has not been necessary." 82
In other words, the Ministry had never tested cattle feed because there was no evidence of wrongdoing. And if you don't look, you don't find.
On March 16, the ministry of agriculture was asked an all-too-explicit question in parliament by MP Ron Davies. Would he now ban the sale of those organs from all cows and sheep that are known to harbor the infectious agent? The parliamentary secretary to the Ministry of Agriculture made it clear that they had no intention of taking any such action. In justification, he presented two arguments. First, carcasses of BSE-suspected cows were already being destroyed. Second, scrapie had been present for two hundred years "without any evidence of a risk to humans." Therefore, it would not be "appropriate" to ban these organs from sale.
But, he was asked, the Southwood committee recognized that there
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was a danger to human health from the consumption of infected organs. And as far as scrapie was concerned, now that it had demonstrated that it can leap across the species barrier (implying a dangerous new mutation), surely this should mean that all organs that act as a reservoir of infection should now be banned from sale? Mr. Thompson disagreed, reiterating that "the Southwood report concluded that it was most unlikely that BSE would have any implications for human health." 83
This issue was yet another hostage to fortune, when the government abruptly decided, just four months later, to reverse its policy and ban cow offal from sale. In retrospect, it seems obvious that policy was being made "on the hoof." As one policy position after another became untenable, it was unceremoniously dumped.
On April 13, Mr. Thompson was asked whether he would introduce restrictions on the movement of calves born to cattle infected with BSE. Mr. Thompson said he had no such plans. This hygiene measure was important, because as long as there was a possibility of "maternal transmission" of BSE (i.e. from cow to calf) the transport of BSE-infected calves around the country might spread the disease.
Again, this reveals an extraordinary inconsistency in the government's policy. One of their key policy justifications was the similarity of BSE to scrapie. Since scrapie hadn't infected humans—they argued—BSE wouldn't, either. But scrapie was clearly transmissible from mother sheep to lamb—there was no doubt at all about this. As Dr. James Hope explained: "In a flock of sheep, the disease is transmitted principally from mother to offspring, that is, from ewe to lamb. That's not to say that it is a genetic disease. We believe infection either occurs in utero before birth, or immediately after birth via the placenta. The placenta is highly infectious, and poses a threat to the newly born lamb and other members of the flock." 84
The following day, evidence emerged that diseased cattle were being sent to slaughterhouses; Mr. Thompson stated in reply to a question from MP Ron Davies that forty cases of BSE-infected cows were detected in abatoirs. 85 No one could say, however, how many cows had slipped through undetected.
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THE FIX
In May, the Women's Farming Union added their voice to rising public demands for a complete ban on the use in any food products of brain and spinal cord material from cows and sheep. 86 The government must take steps, they said, to ensure that BSE and scrapie could not be spread through the food chain.
The government's position had now become universally discredited. An opinion poll for Marketing magazine revealed that only 2 percent of the population believed the government completely on matters of food. 87 The "no evidence" defense was now seen by most people for what it was: a sad and pathetic attempt to keep people buying the dubious products of the British meat industry.
The Southwood committee had spawned another committee, under the chairmanship of Dr. David Tyrell, a retired virologist. This time, its members included scientists with experience of spongiform diseases. Again, they worked with commendable speed, and presented a report to the government in June. Disgracefully, it was not made public for seven more months. 88
However, a few days after receiving the (still secret) Tyrell report, the government abruptly reversed its position on the sale of offal, and a total ban was announced on the sale for human consumption of all cow's brain, spinal cord, thymus, spleen, and tonsils. It was a victory, of sorts. One of the problems was that the ban would not come into effect for five more months in England and Wales, and in Scotland not for seven months. Said Dr. Hugh Fraser, a neuropathologist at the Institute of Animal Health, in Edinburgh, "They could have introduced a ban six months ago. They ought to have a ban as soon as possible. It doesn't seem right to delay it." 89
While he welcomed the ban, Member of Parliament Ron Davies, who had asked so many penetrating questions in the House of Commons, demanded more drastic and immediate action—such as random testing on cow's brains in slaughterhouses to determine the true size of the epidemic. This eminently sensible measure would be steadfastly opposed by the government.
There was no denying that it was a fix. Just three months earlier,
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they had told the House of Commons that a ban on the sale of offal would not be "appropriate." Now, it looked very "appropriate," indeed. But would it be sufficient to reassure an increasingly leery public?
THE COWS COME HOME
Nineteen ninety was the year that the cows came home to roost, or whatever it is that cows of ill omen do. As Professor Richard Lacey wrote, "During the last weeks of 1989 and early in 1990, findings of spongiform encephalopathy in, first, zoo animals such as antelopes, and then domestic cats, were published completely invalidating the Southwood committee's hope that BSE was a 'dead-end host,' that is, it would not spread beyond cattle." 90
So the key question was no longer "can BSE spread to other species?" but rather, "how many other species can it infect—and is homo sapiens one of them?"
A few days into the New Year, a report from trading standards officers revealed that cattle infected with BSE were still being sent by farmers to market—hardly surprising, in view of the low level of compensation being offered by the Ministry of Agriculture. Flying in the face of common sense, a Ministry official commented that compensation was "not an issue" in safeguarding the public from BSE-infected animals. "We have no evidence," the official all-too-predictably commented, "to suggest that farmers are dishonestly sending animals to market knowing they are infected." 91
Nineteen ninety was also the year of the spin doctor. From now on, the disquieting results of animal "transmission" experiments would start to emerge. Yet, with sufficient ingenuity, even the worst results could be made to seem encouraging. For example, in early February, results were published showing that BSE was capable of being transmitted from one cow to another. 92 Gloomy though this might at first seem, a positive "spin" could point out that the cattle concerned were injected with infected material, and this artificial technique would never occur naturally. When another experiment showed that mice (a different species) could contract BSE simply by eating infected cow
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brains, it was pointed out that the amount given to the mice (.32 ounce) was proportionately far higher than the amount likely to be eaten by a human being.
Well, it was supposed to sound like good news.
"SO WHAT?"
In February, the investigative television program World in Action examined BSE and included a pugnacious interview with Britain's food minister, David Maclean. 93 He gave a truculent performance, but it must have done little to reassure the public that their food was in safe hands. "Your critics say that meat inspectors simply aren't as qualified as vets to spot BSE suspect cattle at abattoirs," commented the interviewer.
"Well, maybe they aren't," declared Mr. Maclean. "I wouldn't expect them to be as qualified as vets; vets after all, do a five-year training course. I wouldn't expect them to spot them. So what?"
"Well," said the interviewer, "they're missing a good many BSE-suspect cattle, it is suggested."
"Well, so what?" snapped Maclean.
The thrust of his argument was that since the most suspect organs from all cows were now being removed at slaughterhouses, it didn't matter if some BSE-infected cattle were reaching the slaughterhouses undetected. "We're cutting the offals out of every cow, not just the BSE suspect ones, every single cow," he said. "And that's the final preventative measure."
But the program also included evidence from an experienced environmental health officer that graphically revealed that this "final preventative measure" was by no means the absolute guarantee of safety the government evidently hoped it would be. "When you split down the carcass," he said, "there will be bits of the central nervous system tissue that get scattered all over the rest of the meat. And when the carcass is sawn down, what they do is to hose that off. But again, that in itself is a compromise, because how do we know we get rid of it all? And how do we know what we produce is satisfactory? The whole animal is full of nerves; it's impossible to remove it all. It is the job of my meat inspectors to make sure that none of the banned offal gets
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through. But there will be some central nervous system that is left behind that is not covered by the banned offal, anyway."
"So suspect tissue is going into the human food chain?" asked the interviewer.
"Yes, certainly," was the unequivocal reply.
HEAVY PETTING
In April of 1990, as the number of detected cases of "mad cows" passed the 10,000 mark, the government announced the commissioning of a study to examine the connection between BSE and Creutzfeldt-Jakob disease in humans. 94 This action was taken at the behest of the Tyrell committee's report, which stated, "Many extensive epidemiological studies around the world have contributed to the current consensus view that Scrapie is not causally related to CJD. It is urgent that the same reassurance can be given about the lack of effect of BSE on human health. The best way of doing this is to monitor all UK cases of CJD over the next two decades." 95
Professor Lacey was scathing: "In two sentences, the government's intent is revealed in absolute clarity. Its action is intended somehow to reassure, rather than to take any curative action." 96
What happened next was totally unforeseen. If an evil alien intelligence had indeed been plotting the next move of the infectious agent, it could not have contrived anything better than what followed: A cat called Max died.
The British, as is widely known, are besotted with their pets. Although we are content to allow our food animals to live mean and miserable lives—out of sight—we will not tolerate any insult or injury to our beloved companion animals. So when the first pet cat died from a uniquely distinctive BSE/scrapie-type disease, the nation was appalled and outraged.
With hindsight, it was entirely logical that, if the infectious agent was present in cattle feed, the same infectious material could also be present in pet food. However, the reality of the pets actually dying, and all the negative public relations implications, doesn't seem to have been considered—there hadn't even been a routine "no evidence" statement from the government. But once the diagnosis was made,
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officials acted quickly to put this right, saying there was no evidence "at this stage" of a link with pet food or, indeed, with BSE. 97
No evidence. Remember those two words. Whenever you hear an official spokesperson use them, run as fast as you can in the opposite direction.
Remarks made by the president of the British Veterinary Association raised the possibility that many more cats might be infected, when he was quoted as saying, "Vets are presented with cats showing nervous disorders like this one every day. Some can be treated, some can't and have to be destroyed. But in 90 percent of cases when they do have to be put to sleep owners don't want us to carry out a post mortem." 98 Wisely, the Pet Food Manufacturers Association had already advised its members not to include cattle offal in their products, but in view of the long incubation time of spongiform diseases, there could be no guarantee that many more cats would not subsequently be discovered to have "mad cat disease."
There was now something close to a state of panic in Britain. Within days, beef had been removed from the menus of more than 2,000 schools across the nation. The parliamentary opposition called upon the beleaguered minister of agriculture to take immediate further action or to resign. In an amazing public admonishment, a former chief veterinary officer broke the customary silence imposed on civil servants to lambaste successive governments' policies concerning the recycling of sheep and cows in cattle feed: "No one was more alive to the potential risk involved in tampering with the eco-system than I was," said Alex Brown. "I continually drummed it into everyone around me that we should never, never forget that nature has a right to do funny things to man. You should also never dismiss the unknown, because it is unknown." 99
That, of course, is precisely what officials had been doing when they continually asserted that there was "no evidence" of any risk. Clearly, the government and the meat trade were losing the propaganda war, and they had to counter attack. The Meat and Livestock Commission decided to launch a $1.4 million advertising campaign. "It is not a response to the latest scare over BSE," said their marketing director. "It reflects our concern about the general pressure to eat less meat." 100
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Colin Cullimore, managing director of the Dewhurst chain of High Street butchers, laid into Professor Lacey. "Professor Lacey is being alarmist," declared Mr. Cullimore to The Times. "He is a scientist, but he is making statements without any evidence." 101
In a broadcast to the nation, the minister of agriculture, John Gum-mer, condemned "scare mongers." "The public has absolute confidence that I am not going to be pushed off what is the right action merely to curry favour with one or two people," he said. 102
In parliament, David Maclean, the food minister, lashed out at "so-called experts" who failed to submit their evidence, and another backbencher complained of "a bogus professor." 103 While speaking in the British Houses of Parliament, members are protected by parliamentary privilege against the laws of libel.
IMPROPER SUGGESTIONS
On Wednesday, May 23, 1990, the Agriculture Committee of the House of Commons opened its proceedings on BSE. For the minister of agriculture, it was to be a fateful day. As an astute politician, John Gummer must have realized the crucial importance of a favorable verdict—if the committee vindicated his handling of the crisis, it would provide him with some sorely needed political backing. But if, on the other hand, it censured him, then who knows what might happen?
There was always the possibility that events could take a disastrous turn, but as John Gummer prepared to testify that afternoon, he must have felt a certain degree of quiet confidence. He was not, after all, alone. On his left sat Keith Meldrum, chief veterinary officer at the Ministry of Agriculture. Next to him sat Elizabeth Attridge, head of the Animal Health Division of the ministry. And on the minister's right was Dr. Hilary Pickles from the Department of Health, joint secretary to the Tyrell committee. All in all, a high-powered team, combining political acumen with scientific erudition. It would be difficult for things to go too far wrong.
The minister kicked off with a long introductory statement, expressing his pleasure with the committee's decision to hold an inquiry, outlining the course of the disease since its detection, and summarizing the government's response. It was, as one would expect,
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executed with proficiency, and the formal nature of the proceedings precluded any awkward interruptions or cross-examination until the minister had finished speaking.
He started well. Although Mr. Gummer could never be accused of Churchillian oratory, his mind was sharp, and the structure of his speech was logical, stressing the government's deep concern, its swift response to the crisis, and the firm grasp his ministry had over the problem. It was a good beginning, and he must have felt increasingly confident.
Perhaps he should have left it there. He certainly could have done that, because he had already said enough to create a favorable impression. But he didn't. He was well into his stride when something altogether astounding happened:
The official line had always been that, since there was "no evidence" that scrapie could infect humans, it therefore followed that BSE couldn't infect humans. This was a central tenet of the government's policy position. But that afternoon, John Selwyn Gummer, minister of agriculture, went much, much further than that. This is what he said: "The plain fact is that there is no evidence that BSE poses any risk. Some may argue that BSE is a new disease, so how can we be so sure. Well, there is good historical evidence because BSE is very similar to sheep Scrapie which has been in the sheep population for over 250 years without any suggestion that it poses a risk to humans. Neither have extensive studies shown a link between Scrapie and the human disease CJD." 104
To the assembled members of the parliamentary committee, it must have sounded very persuasive. As Mr. Gummer spoke, flanked by experts, he must have appeared both impressive and credible.
There was just one problem: He was absolutely wrong.
SCRAPPING OVER SCRAPIE
Whatever possessed Mr. Gummer to make such a breathtaking assertion, we may never know for certain. He could just as easily have used the formulaic weasel words so beloved of politicians—"no conclusive evidence," "no proof," and so on—which would have adequately
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conveyed his message without putting his neck on the line. But he didn't.
He'd now gone on record, before a committee of the House of Commons, claiming that scrapie had existed in the sheep population "for over 250 years without any suggestion that it poses a risk to humans." "Suggestion" is defined by the Oxford English Dictionary as "the putting into the mind of an idea . . . an idea or thought suggested, a proposal." 105 In effect, he seemed to be implying that the very notion that scrapie might pose a risk to humans was so inconceivable that no scientist would even propose the idea.
But this was rubbish. For at least fifteen years, there had indeed been "suggestions" from scientists that scrapie might play a part in the development of CJD, Creutzfeldt-Jakob disease. It was unthinkable that the minister's experts were not aware of this. But that afternoon, the experts were on Mr. Gummer's team. They were there to support him, not to cross-examine him.
It is, of course, conceivable that Mr. Gummer had been misinformed by his expert advisers. This is highly unlikely, however, as a close examination of his words reveals. For immediately after claiming that there hadn't been "any suggestion" that scrapie posed a risk to humans, he alluded to "extensive studies" examining the link between scrapie and CJD. The obvious question that arises from this is: if there hadn't been "any suggestion" that scrapie might pose a risk, why had "extensive studies" been performed? There is a conspicuous error of logic here.
What would have happened that day if the Agriculture Committee had taken steps to widen their inquiry and examine this new area in detail? We can only speculate, of course. They might have come to the same conclusions, in any case. Then again, they might not.
From the government's point of view, the worst possible outcome of the committee's inquiry would have been a failure to exonerate their conduct of the BSE disaster, coupled with a widening of the inquiry into the related area of scrapie and sheep. Given the existing high level of anxiety among the British population, it was conceivable that such a chain of events could have precipitated a governmental crisis of uncontrollable dimensions.
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Perhaps in his desire to avoid opening this particular can of worms, Mr. Gummer simply went over the top, and abandoned the careful language of politicians. If so, it was an astounding mistake, and he was indeed fortunate not to have been challenged about it.
Until this book came along.
THE FIRST "SUGGESTION"
The first major "suggestion" that sheep scrapie might be linked to Creutzfeldt-Jakob disease in humans was presented to thousands of the world's scientists on November 29, 1974. 106 That day, an issue of the widely read journal Science was published, carrying a letter signed by six distinguished scientists, including D. Carleton Gajdusek, the kuru expert and later, Nobel prize winner.
The letter was in response to a research paper published in the same journal earlier in the year. The authors of the earlier paper were intrigued by the preponderance of CJD among certain population groups within Israel. Jewish families who had emigrated from Libya were particularly susceptible—up to seventy-eight times more likely to suffer from CJD than the general population. In response to this strange finding, the six scientists wrote:
"This finding may be related to the dietary habit of eating sheep's eyeballs, which are a gastronomic delicacy among Bedouin and Moroccan Arabs and also Libyans. A disease of sheep, Scrapie, has clinical and histopathological features similar to those of CJD ... If the CJD agent is found in the cornea, retina or optic nerve, the ingestion of eyeballs of sheep harbouring the Scrapie agent might possibly lead to the development of CJD in susceptible individuals and thus account for the high incidence of the disease in Libyan Jews." 107
This "suggestion" wasn't simply idle speculation. It had recently been tragically proven that CJD could be transmitted from one person to another when the recipient of a corneal transplant, unwittingly taken from a donor suffering from CJD, subsequently contracted CJD and died from it. Therefore, if the CJD agent was present in human eyeballs, it might also be present in sheep's eyeballs.
One of the authors of the original study replied to this suggestion with some interesting evidence: "We knew that brain and spinal cord,
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mainly from sheep, was a delicacy among Libyan Jews," he wrote. "Inquiries even revealed that a favourite method of preparation is light grilling, which could conceivably leave an infectious agent viable." 108
However, he went on to say that having considered the idea, they then rejected it, on the grounds that the consumption of sheep's eyeballs was not limited to just the Libyan Jewish population, "so we deleted reference to it in our final manuscript," he explained, concluding that "brain is a more likely source of the putative CJD agent than eyeballs."
And so the ongoing debate began—not in public; but among scientists, and in the rarefied pages of professional journals. Evidence would be produced in favor of the theory, and evidence would be produced against it. But no one could now claim, with any truthfulness, that there had not been "any suggestion" that scrapie posed a risk to humans.
ON THE TRAIL
Let's stay with the scrapie/CJD story for a little—not to further discomfit the poor Mr. Gummer, but so that we can understand some aspects of these enigmatic spongiform diseases.
After the publication of the initial report in Science, more research was conducted into the Libyan Jewish population. It produced more tantalizing evidence, but not clear proof. One piece of research, for example, showed that the vast majority of CJD patients had indeed been known to consume sheeps' brains—but so did other "controls," without apparently succumbing to CJD. 109 What did this mean?
It simply meant that a clean-cut, cause-and-effect relationship could not be easily established. While it was notable that the CJD sufferers were more often exposed to animals than the control group— and, significantly, they ate brains that were far more lightly cooked—this was not in itself strong enough evidence. Another study summarized it like this: "The results suggest either a common source of exposure or a genetic influence on susceptibility to the virus." 110
The science of epidemiology, which is really detective work by numbers, is at its strongest when a clear cause-and-effect relationship
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can be proven. In order for the scrapie-CJD theory to be proven beyond doubt, it would have to be shown that people suffering from CJD differed significantly from the general population in their exposure to the scrapie agent in sheep meat. As long as there were people in the population who didn't contract CJD, but who were similarly exposed to sheep meat, it could not be conclusively demonstrated that scrapie caused CJD. So, although the evidence so far didn't prove the connection between scrapie and CJD, it didn't disprove it either.
Let's take a moment to consider these six links in the chain of disease transmission:
1. Characteristics of the agent
2. A reservoir
3. Portal of exit
4. Mode of Transmission
5. Portal of entry
6. Suspectibility of host
In a way, this chain looks rather like a game of Russian roulette— you have to be rather unlucky to lose and become infected. Before anything can happen, the infectious agent itself must be one of a strain capable of causing disease (there are several different scrapie strains). Then, there has to be something that acts as a reservoir of infection. This in itself is a powerfully suggestive argument in favor of a connection between scrapie and CJD, because CJD would have died out by now if it was purely confined to human beings—there is almost certainly a natural reservoir of it outside our own species, which periodically reinfects us when conditions are right.
Next, there must be a way of getting the disease out of the natural reservoir—in the case of scrapie, the most infectious parts of the sheep are the brain, placenta, spleen, liver, and lymph nodes. Then, there has to be a method of carrying the infection to the new host. Well, in the case of sheep, that's easy enough—we eat them. So far, so good— or bad, as the case may be. But all this still isn't enough to infect the host. Two more essential steps are necessary:
The first is the route into the host itself. Now, we know that the effectiveness of different routes of entry to the host are extremely vari-
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able. At one end of the spectrum, we know that scrapie can sometimes be transferred very easily from one sheep to another simply by allowing the healthy sheep to graze on pasture previously grazed on by infected sheep—no other contact is needed. 111 At the other end of the spectrum, it has been demonstrated that sometimes only direct inoculation into the brain with infected material will succeed in transferring infection. So between these two extremes, there is a huge variety of routes, some far more successful than others. This is a significant point, because there is evidence to suggest that eating scrapie-infected meat may not, in itself, be sufficient to produce an infection—there may also have to be some kind of accidental inoculation, such as biting the skin of the mouth at the same time, or lesions of the lips, gums, or intestines.
Finally, there has to be an existing susceptibility to the disease in the new victim. Some breeds of sheep are far more susceptible to scrapie than others. By implication, some humans may be more susceptible, too. As we will see later, this is the "joker in the pack," because Scrapie/CJD is peculiar in having both a genetic and an infectious component. Tricky stuff, indeed.
You can see that there are many, many possible factors that can affect the transmission of disease—and its subsequent detection. Because of this, it is not always possible to tease out a clear cause-and-effect relationship from the numbers. For example, in one study of thirty-eight American CJD patients, it was established that at least ten of them had eaten brains within the previous five years—apparently, a very significant finding. 112 However, nearly as many people in the "control group" had also eaten brains, and didn't get CJD.
"The chance of a person's getting the disease depends on a complex sequence of events . . . ," one scientist commented, while reviewing the results. "It is important to remember that exposure to a suspected mode of transmission may not be enough to result in disease, and some ingenuity in the method of inquiry will have to be introduced. For example, in this study, a high but equal proportion of both patients ate brains. What could be critical is that the patients may have experienced some coincidental events, such as concurrent trauma or acute respiratory infection which caused a break in the skin or mucosal lining thus allowing the CJD agent a portal of entry." 113
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The fact is, even with the best team of scientists available, it could be next to impossible to ever provide the sort of conclusive epidemiological proof that would convince everyone that scrapie can cause CJD. One major stumbling block is the sheer length of time between infection and onset of disease: how many people can accurately remember what they had to eat twenty years ago? Also, bear in mind that many CJD patients are not properly diagnosed until after death, and scientists have to question their next of kin—which makes it even more difficult to get accurate responses.
There are problems, too, simply recognizing CJD. Until 1979, the International Classification of Diseases (a system used to codify causes of death) didn't even include a specific category for Creutzfeldt-Jakob disease. 114 In Britain, approximately 75,000 people die every year from "dementing" diseases. Yet the official statistics show that only thirty to forty people die from CJD. There is good evidence to believe that the true figure is far, far higher—probably in the region of 9,000 cases. 115
And here's yet another problem. In America, it has been found that areas with the largest number of reported outbreaks of scrapie (Illinois, Texas, Indiana, Ohio, and California) have no more cases of CJD than the national average. Is this reassuring evidence? By no means. It actually tells us very little at all. As one reporter commented, "Such a comparison is of limited value, since Scrapie-infected material may have been widely disseminated throughout the country in processed meat." 116
Today, most of the food we eat has been transported hundreds, sometimes thousands, of miles. Therefore, a local outbreak of scrapie might result in a cluster of CJD cases far away in another continent!
Another report reveals that we can't even be certain that sheep with scrapie will be accurately diagnosed. Examining the marketing of sheep in Pennsylvania, scientists concluded that "sheep were usually marketed before central nervous system signs of Scrapie were expected to appear"; that "opportunities to detect the disease were limited"; and "sheep producers in the area knew little about Scrapie despite the fact that the disease has been reported in the area." 117
All these difficulties present formidable obstacles to epidemiologi-
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cal surveys. In France, a twelve-year study of scrapie in sheep revealed that the disease had been diagnosed "in virtually every region where sheep are raised." 118 It also found that lamb consumption among some growing population groups correlated with an increasing frequency of CJD. A year later, a continuation of the same study still found that "there is a correlation between lamb consumption and CJD mortality rates in different nation-wide population categories." 119
However, five years later, the scientists had identified a total of 329 patients dying of Creutzfeldt-Jakob disease, but were unable to conclude there was a clear connection with lamb consumption, or with any other single factor. 120 Such equivocal evidence is hard for scientists to come to grips with. Therefore, when something more substantial comes along, it is eagerly seized upon, and previous theories are forgotten. And that is precisely what happened next.
BAD GENES?
"Clusters of CJD have long been known," declared The Economist magazine two months after Mr. Gummer testified to the House of Commons Agriculture Committee. "The most famous was among some Libyan Jews in whom CJD was almost 40 times more common than normal. Since they ate sheep, it was thought that Scrapie might be to blame. Further research showed that the sufferers were related. . . . Although it may be worrying that such clusters of CJD exist," the writer explained, "the good news is that they seem to have been caused by bad genes, not bad mutton." 121
Well, maybe it wasn't such good news, after all. Initially, it had been proposed that there was a simple family connection between the Libyan Jews who suffered from CJD—in other words, it was a hereditary disease. Subsequent work, however, failed to confirm this. 122
What was subsequently established by genetic detective work was that the Jewish CJD patients displayed a specific genetic mutation. 123 So were "bad genes" the cause of CJD? The answer would come from the largest—and for us the most worrying—cluster of CJD cases yet discovered; right in the middle of Europe.
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A PLAGUE IN SLOW MOTION
Cases of Creutzfeldt-Jakob disease among Libyan Jews were forty times more common than normal—and that was considered to be extraordinary. Today, in Slovakia, an epidemic of CJD is developing. I use the word epidemic deliberately, because in certain areas, the incidence of CJD is more than three thousand times the ordinary level. 124
It seems strange to think of an epidemic with an incubation time measured in decades. When people drop like flies—from cholera, for example—the drama momentarily hits the headlines, and we are all horrified, until we forget about it. But with CJD, there is no instant, three-minute tragedy, conveniently prepackaged for the evening news bulletins. There is no news angle for a plague that is running in slow motion.
Whatever is developing in Slovakia is a matter of intense interest, and deep concern, to many scientists. Some experts believe that we are now seeing the beginning of a worldwide epidemic of "kuru virus"— encompassing the sudden appearance of BSE, an upsurge in scrapie in sheep, and CJD in humans. "We have a major problem in human disease," grimly warns one authority. 125
When a conventional epidemic strikes, time is the enemy. You need time to identify the causative agent, time to study it, and time to develop countermeasures. When the period between infection and death may be just a few days, you never have enough time. But that's not the case with CJD. Which is why the Slovakian epidemic is the best-studied, most investigated outbreak of CJD ever. In the past few years, we have learned more about the cause of CJD than we've ever known before.
COMPELLING NEW EVIDENCE
This chapter began with a film plot in which Russian and American scientists battled to save the world from annihilation. A real-life parallel has been going on in Slovakia, as both Americans and scientists who were formerly under Communist jurisdiction now cooperate to comprehend the nature of the epidemic now in progress. Here is a summary of this little-known but crucial research work, to date:
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The epidemic has two centers. One is located in the rural Lucenec area of south-central Slovakia, with some cases being reported from across the Hungarian border. The other is based further toward the north, in the Orava area, to the west of the High Tatra mountains on the Polish border. The two areas differ significantly in some key respects. In the south, the disease progresses steadily, continuing to claim about the same number of people every year. In the north, however, it suddenly erupted in the late 1980s—two small villages, with a combined population of less than 2,000, have had more than twenty cases of CJD in the last three years alone. 126 Once again, initial research first suggested that the disease had a genetic origin. 127 Nine CJD victims from the north, and six from the southern cluster had their DNA sequenced, and it was found that they all had a similar mutation. This discovery led some scientists to claim that CJD was "caused" by a genetic mutation—back to the "bad genes" theory described above. However, subsequent evidence has shown that as a comprehensive explanation, it simply isn't tenable, for the following reasons: Genetic screening has established that the mutation in question was present in people living in the northern Orava region at least as far back as 1902, and probably much earlier. Yet it was only recently—in 1987—that CJD suddenly exploded in frequency there. Obviously, if "bad genes" was the root cause of CJD, there would have been cases of CJD as long as people had been carrying the genetic mutation. This clearly points to another "triggering" factor in the environment, such as the emergence of scrapie.
When scientists studied families in which CJD had claimed more than one victim, they found that CJD occurred more or less at the same time—but not at the same age. If the disease was purely genetic, it would be more likely to occur after a certain number of years. This evidence also suggests that suddenly, an environmental source of infection appeared, with tragic consequences.
After extensive genetic screening, it was established that many people could carry the genetic mutation, but remain perfectly
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healthy. 128 Further research work with CJD outbreaks in Chile has now established that among one identified group of people with the mutation, only half the expected number actually developed CJD. 129 This is very convincing evidence that an environmental factor triggers the disease in those susceptible to it.
• A case history illustrates the importance of an environmental factor with great clarity. Three children were all found to be carrying the genetic mutation. Two of the children grew up in their birthplaces, within the southern cluster of CJD. Both of these children subsequently contracted CJD and died. The third child, however, didn't contract CJD—even though she carried the mutation. The difference was that she was taken away from the area while still an infant, and lived and grew up in Bratislava, well outside the danger area. 130 But why should there be "danger areas," in any case?
• The answer to this lies in recent agricultural history. In an attempt to stimulate the Slovak sheep farming industry, sheep were imported from 1970 onward from England and France— and the breeds chosen (He de France and Suffolk) are both highly susceptible to scrapie. 131 Furthermore, careful research work has revealed that most of these sheep went into regions that are now suffering from CJD.
• The evidence becomes more incriminating still when you examine the jobs that the CJD patients had. Well over half of them worked in livestock farming or meat processing. 132 Further laboratory work has now confirmed that scrapie definitely exists in these flocks of sheep—and, equally troubling, scrapie infection has now been identified there in sheep not manifesting any clinical symptoms of the disease. 133
To summarize—this evidence strongly supports the theory that the most recent epidemic of CJD is the lethal result of genetically susceptible people being exposed to the scrapie agent in sheep.
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NEWS FROM WONDERLAND
Early in 1992, it seemed as if the "all clear" had sounded.
"Beef given a Clean Bill of Health," proclaimed the headline in the Meat Trades Journal. 134 "The results of the latest batch of tests on BSE suggest the disease cannot be passed from cattle to humans." The report continued, "British beef has been given a clean bill of health by a government scientist claiming tests on monkeys may have proved BSE cannot be transmitted from cattle to man. ... 'I am absolutely convinced BSE can't be transmitted easily from cows to humans,' ' the government scientist was quoted as saying. " 'I don't believe the meat of any cow is a risk to man and am certain that the meat arriving at any butcher always has been and still is fit to eat.' K
Reassuring words, indeed. Based on an experiment that involved transmitting BSE to marmosets, small monkeys belonging to the same biological family as humans, two marmosets were injected with tissue taken from BSE-infected cattle, and another two were injected with material taken from scrapie-infected sheep. The two marmosets infected with scrapie both died, but the other two lived on. "I feel certain that the monkeys have passed the danger period," the scientist was quoted as saying. "I would have no worries if butchers told any customers still refusing to eat beef that there is little or even no chance of them developing the disease."
Just two months later, the Meat Trades Journal carried the following stark, doom-laden headline:
"Primates are affected by BSE." 135
What had happened? Why, one of the two BSE-infected marmosets had died, and the other one was only expected to live for a few more weeks. Yes, they'd both got Mad Cow Disease.
So did this change everything? Did the government scientist quoted above now consider that BSE was more of a threat to human health? Not at all. The article quoted the scientist as now saying; "We now know that BSE is even less of a risk."
And the Ministry of Agriculture commented (Do I really need to write this for you? I mean, by now, you know what's coming, don't you?) that there was no cause for concern about human health. 136
So that was all right, then.
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MILESTONES ON THE ROAD TO HELL
And the saga continued:
• In May 1994, Germany threatens to ban British beef imports but retreats under political pressure.
• In October 1994, the national Creutzfeldt-Jakob disease surveillance unit announces, "We see no evidence of an emerging CJD epidemic."
• In October 1995, the Spongiform Encephalopathy Advisory Committee orders an investigation into the cases of two British teenagers who developed CJD.
• In December 1995, Prime Minister John Major says, "I am advised that beef is a safe and wholesome product. The Chief Medical Officer's advice on the point is clear: there is no evidence that eating beef causes CJD in humans."
• In February 1996, the food minister, criticizing a "British beef could kill" campaign, says, "This campaign is outrageous."
• In March 1996, the agriculture minister tells Parliament, "British beef can be eaten with confidence." 137
With confidence.
• On Wednesday, March 20, 1996, the British government finally admitted that Mad Cow Disease could be passed to humans by eating beef.
• The official report into the Mad Cow disaster states, "The Government did not lie to the public about BSE. It believed that the risks posed by BSE to humans were remote. The Government was preoccupied with preventing an alarmist over-reaction to BSE because it believed that the risk was remote. It is now clear that this campaign of reassurance was a mistake."
So that was that.
Very gentlemanly. Very British. And no one carries the can.
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EARTH SAVED? EARTH DOOMED?
I wish I could tell you what the final impact of Mad Cow Disease on the human population will be, but I can't. No one can. Projections by British experts in 2000, based on recorded deaths so far, suggest that as many as 500,000 Britons could die over the next thirty years. 138 Vegetarians and vegans can't afford to be smug or consider themselves immune: meat products are so ubiquitous in our society that it is inevitable that we will consume them in one way or another, either as gelatin, in vaccinations, as a blood transfusion, or in a host of other ways.
Is Mad Cow Disease present in America right now? Officially, no. But data from the U.S. National Veterinary Sciences Laboratories BSE Surveillance Program from 1990 to 2000 show that of approximately 900 million cattle slaughtered, only 11,954 brains (approximately 1 in 75,000) were examined for BSE. And brain examinations have generally been prompted by the presence of neurological symptoms. However, the symptoms of BSE do not commonly manifest in cattle until they are about five years of age, which is after the usual age of slaughter. For example, most U.S. dairy cows are slaughtered before four years of age, when even an infected cow may appear healthy. In the U.K., 70 percent of dairy cows remain alive past this point, making identification of infected animals much easier. 139
A number of American experts believe that it is probably here, at low levels. 140 How did it arrive? Unfortunately, there are a multitude of ways. For example, British export statistics show that twenty tons of "meals of meat or offal" that were "unfit for human consumption" and probably intended for animals were sent to the United States in 1989. In an exception to the import ban, many health supplements have contained glandular material from animals whose health status could not be determined. 141 Tourists to Europe would certainly have been exposed to infected beef, just as the locals were. Military records reveal that millions of U.S. military personnel stationed in Europe before 1996 would have eaten British beef on base during the height of the epidemic. 142 As I'm writing this, today's New York Times reports that U.S. pharmaceutical companies have been using animal ingredients from cattle raised in countries where there is a risk of Mad
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Cow Disease, even though the U.S. Food and Drug Administration asked them not to. 143 In today's global economy, no nation is an island, and the arrogant failings of the British political administration don't jeopardize just the health of Britons: they potentially affect everyone in the world.
We also know that CJD is seriously underdiagnosed at present, the most common misdiagnosis of CJD being Alzheimer's disease. 144 In fact, the brains of the young people who died from the new CJD variant in Britain look like Alzheimer's brains. 145 Four million Americans are currently affected by Alzheimer's; 146 it is the fourth leading cause of death among the elderly in the U.S. 147 Epidemiological evidence suggests that people eating meat more than four times a week for a prolonged period are three times more likely to suffer a dementia than longtime vegetarians. 148
My own experience of watching the progress of this epidemic is that we would be very, very foolish to write it off as gone away. Time and time again the British government seems to have done exactly this, and like a monster from a horror movie, the thing you think you've killed gets right back up and keeps coming at you.
So what can we do?
WHAT AMERICANS MUST DO
"Our government has been frighteningly slow to react to the very real threat of CJD in America," said Dr. Neal Barnard in a critique of U.S. government policy in January 2001. Dr. Barnard is president of the Physicians Committee for Responsible Medicine, and he talks a lot of good sense. He continued, "The protective measures taken so far are grossly insufficient. We should learn from Europe's mistakes and implement tough precautionary measures—now, before it's too late." Here are his five recommendations for protecting the American public against Mad Cow Disease:
1. Ban the use of animal-derived livestock feeds for any species, given the likelihood that animal by-products will, in turn, be recycled to ruminants (that is, cows, sheep, and goats).
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2. Prohibit animal by-products in all medications, supplements, and cosmetics.
3. Label all foods containing animal by-products (such as gelatin or "natural flavorings"), indicating both the presence of animal by-products and the species of origin.
4. Provide warning labels on all foods that carry a risk of CJD, using standards similar to those for tobacco and alcohol products.
5. Institute comprehensive monitoring programs to check for diseased animals and humans in the U.S. 149
And what can you, as an individual, do? The Mad Cow Disease crisis is a stupid, self-inflicted epidemic caused by the greed of an agricultural system that puts profit ahead of all other considerations. If we turn a naturally vegetarian species, the cow, into an intensively reared cannibal, then something nasty is likely to happen. It did, and we're only beginning to count the cost. My advice to you is simple: go vegan. You will greatly reduce your risk of coming into contact with infected material, and you will also stop supporting a greedy, grossly unnatural, and deeply unethical food production system that is good for neither man nor beast.
PIG TALES
As a kid, I'd come to the conclusion that my personal obstinacy in regard to meat eating was a lone and unique eccentricity, an abnormality in a world where meat eating was the universal rule. I had grown up in close contact with many kinds of animals, and I grew to like them and understand them. This is unusual today; most children now grow up in big cities, and the only contact they have with animals is with pets, or with the processed animals on their dinner plates.
If you have a companion animal, you'll know that he or she has a personality, probably quite a strong one. Actually, all animals have individual personalities; it's just that most of us never have the chance to get to know them.
One snowy January, my parents bought some goslings (baby geese) with the intention of fattening them up and selling them just before Christmas. But a strange thing happened over the next few months: every goose (and gander) got a name, and as I observed them, I became increasingly involved with their rich and complex lives, which are every bit as multilayered as the average human's. There was the "alpha male" (Thomas), who was a typical male chauvinist. Bossy and domineering, he tried to control everything, but in doing so was embarrassingly subject to frequent pratfalls, causing him to lose much of his dignity and prestige. There was Janet, a small and very pretty female who was jumpy and quite literally flighty: flapping her wings in excitement would often lead to unexpected takeoffs, and even more
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bizarre landings, such as the time when she alighted on my mother's head—a major surprise for both of them. And there was Simon, an outcast, raised inside the farmhouse and believing himself to be a human, not a goose. Simon surprised all of us one spring when "he" laid an egg.
Come Christmas, it would have been as murderous to think about sending our geese to market as it would have been to kill a close family member. Yet, when visitors came to stay with us, they always said, "How on earth can you tell them all apart? They look exactly the same!" I could never understand this comment: for me, each goose was clearly and obviously a distinct individual.
Both the geese and the chickens, ducks, and other assorted family members we seemed to accumulate had their own very understandable languages. I quickly learned, for example, the language that chickens used to tell each other where food was found, or the "words" that mother geese use to summon their goslings. To eat creatures that were, in effect, my friends seemed to me to display all the moral superiority of the cannibal. As George Bernard Shaw once remarked, "Animals are my friends, and I don't eat my friends."
I don't know how you feel about these things. You might feel I'm just being squishy and sentimental, and in the real dog-eat-dog world (have you ever actually seen a dog eat another dog?) there isn't time for these cuddly, warm thoughts. Maybe. All I know is, my life as a kid was made richer and deeper from my "friendships" with the animal world, and it's permanently broadened my range of experience. But maybe you're right, and I should have spent my time watching Schwarzenneger videos and playing "killer" videogames, like kids these days do. It might have toughened me up a bit more.
When, many years later, I discovered that mine was not an isolated and freakish persuasion, that countless other people shared my qualms about slaughter, and that vegetarianism had a long and mightily distinguished history, I was frankly astonished. I no longer considered myself to be simply "squeamish": now, I walked in some pretty good company: Da Vinci, Empedocles, Gandhi, Lincoln, Paine, Plutarch, Pythagoras, Schweitzer, Shaw, Tolstoy, Voltaire ... all these and many more were either vegetarian themselves, or resoundingly endorsed the meat-free ethic.
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That vegetarianism was not merely a "food fad," but had a rock-solid ethical basis was indeed wondrous news to me. With this revelation, I began to wonder how any educational system that is worthy of the name can allow children to emerge without at least some basic exposure to the ideas of the great ethical thinkers of history.
PAY ATTENTION—THIS IS INTERESTING
Today, ethics is one of the hottest fields of study in higher education. It's not a remote, academic subject only of interest to professional philosophers: increasingly, the application of practical ethics will determine the future of our world. Just think about a few of the advances that science is on the brink of offering us:
• The chance to permanently alter the human germ line
• The ability of parents to specify a new baby's characteristics just as easily as they might order a Big Mac
• The possibility of life extension offering some of us near immortality
• The creation of artificial life that is to all intents and purposes identical to us
• The likelihood of coming into contact with other intelligent life forms in the universe
Increasingly, the question will not be "can we?" ... It will be "should we?" And that is why the study of ethics is absolutely crucial. Luckily, the basics aren't too hard at all.
Ethical theory can be divided into two main schools of thought: one is called Consequentialist, the other Nonconsequentialist.
These wordy labels disguise ideas that are basically pretty simple (as is too often the case with philosophy). Consequentialist ethics are based on the idea that an action's "rightness" or "wrongness" depends on the consequences of the action. For example, if you steal your friend's watch, thus causing him to miss an important meeting, then the act of stealing would be wrong, because the consequences of your action were detrimental to your friend. However, if your friend never missed his watch, then it might be argued that what you did was not
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wrong, because no negative consequences ensued, indeed only positive ones to you—a "victimless" crime.
Nonconsequentialist theories take a different point of view. They hold that, regardless of the consequences, an action may be either morally right or morally wrong in itself. Stealing, for example, would generally be considered to be a bad thing according to many Nonconsequentialist schools of thought, even if there was no harm as a result. Stealing your friend's watch is wrong, whether he misses it or not.
Now, what is most interesting is this: within both major ethical theories, there are highly developed arguments in favor of vegetarianism—it is not the exclusive property of one or the other major (and mutually antagonistic) school. Let me explain:
Within Consequentialist ethics, we find the doctrine known as Utilitarianism, which had its origins among the British philosophers of the seventeenth and eighteenth centuries. Again, it is a straightforward enough idea, simply expressed in the words of eighteenth-century philosopher Jeremy Bentham, who believed that an individual should seek "the greatest happiness of the greatest number."
Utilitarian philosophers therefore judge an action's Tightness or wrongness by its overall impact on the balance sheet of happiness: if it creates more happiness than suffering, the action is good; but if it creates more pain than pleasure, then it is wrong. Consequently, Utilitar-ianists advocate vegetarianism for the very good reason that the trivial amount of pleasure created by eating meat is more than offset by the huge amount of suffering inflicted on the animal population. Within the Utilitarian school, Peter Singer (who wrote Animal Liberation) is one of its chief modern advocates. Note that Utilitarians rarely talk in terms of absolute "animal rights" or even "human rights." Professor Singer, for example, could foresee certain restricted circumstances in which even vivisection would be right. As he says, "If one or even a dozen animals had to suffer experiments in order to save thousands, I would think it right and in accordance with equal consideration of interests that they should do so. This, at any rate, is the answer a Utilitarian must give." 1 The attraction of Utilitarianism lies in its coherent and flexible basis; it sees morality as a human creation with the aim of increasing the amount of happiness in the world.
Nonconsequentialist ethics, on the other hand, include those philoso-
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phers who argue in favor of animal (and human) rights. Rights are absolute things—they are not subject to a cost-benefit analysis. For example, according to some people, dropping the atomic bomb on Hiroshima shortened the course of the Second World War, and therefore saved lives on both sides. Some Utilitarians might argue that this was on balance a good thing, but those philosophers representing the rights viewpoint would disagree, saying that killing is always wrong, whatever the circumstances or putative benefits. Those Nonconse-quentialist philosophers who advocate vegetarianism (such as Professor Tom Regan, who wrote The Case For Animal Rights) do so on the principle that the basic moral right possessed by all beings is the right to respectful treatment. They also hold that animals, like humans, have inherent value in themselves; they have the potential to lead fulfilling lives, and should be allowed to do so. Where the inherent value of an animal is debased—as, for example, in the case of the degrading conditions in which factory farm animals are kept—then their rights have also been violated. Similarly, if an animal can be either treated fairly or unfairly, their basic right to justice dictates that we must treat them fairly. The attraction of the philosophy of animal rights is that it provides clear and unambiguous guidelines about the way we should treat animals; and anyone who accepts the philosophy of human rights must, logically, also accept the validity of animal rights. If they do not, then they are acting as speciesists, sibling to racists and sexists.
As a little boy of eleven, I knew nothing of these vast ideas. For me, then, and for countless numbers of other little boys and girls who are upset at the thought of killing animals, not eating their carcasses seemed to be the very least one could do. Adults, of course, often resort to trickery in their attempt to make children eat meat. They may stuff it inside a banana-shaped casing and claim it's a "hot dog," or even lie barefacedly to their kids ("the little piggy-wiggy wants you to eat this, darling").
But it's the lies that adults tell to themselves that are the most interesting.
A MIND SPLIT ASUNDER
Schizophrenia is the most common form of psychosis in our society. It literally means "split mind," and it is used to describe an abnormal splitting of psychic functions so that ideas and feelings are often rigidly isolated from each other. For example, a sufferer may express frightening or sad ideas in a happy manner.
Meat eaters also demonstrate a kind of "split mind." When you think about it, the whole point of eating meat is to obtain pleasure (there is no other valid justification). Listen to the conversation of gourmets—folk who often take their pleasures with frightening seriousness—and you will hear people engaged in nothing else but the earnest pursuit of indulgence, as they debate, with great feeling, the comparative delights of such delicacies as veal, goose liver pate, frogs legs, and an endless agenda of even more recondite morsels.
Well, there's nothing wrong with taking pleasure in what you eat. Food is, after all, one of humanity's greatest delights and sources of comfort, is it not?
Indeed it is. But what puzzles me is this. When savoring a tender mouthful of veal, or deliberating over those oh-so-succulent cuisses de grenouille, how do you stop yourself from thinking about the misery and pain that the animal experienced? I mean, doesn't the thought of a baby calf, crying in fear to be reunited with its mother, upset you— just a little? Doesn't it take the edge off your appetite?
Meat eaters do not allow such unpleasant thoughts to interfere with the weighty processes of ingestion and digestion. But actions have consequences. When someone eats veal, the consequence is that the market for veal increases, and more baby calves will be born and live sad and wretched lives.
Yet in the divided mind of the meat eater, no connection between his action and the inevitable consequence has been made, because unpleasant thoughts like that are simply not permitted. And so he or she learns to live in a kind of dream world, where actions don't have consequences, and self-gratification takes precedence over everything.
A split mind.
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THE NAZI INSIDE
"American slaughterhouses," says Dr. Alex Hershaft, a prominent campaigner for animals, "are our Dachaus, our Buchenwalds, our Birkenaus. Like the good German burghers, we have a fair idea of what goes on there, but we don't want any reality checks. We rationalize that the killing has to be done and that it's done humanely. We fear that the truth would offend our sensibilities and perhaps force us to do something."
Does this offend you? Do you think that it is wrong to compare the deaths of the victims of the Nazi holocaust to the way animals are treated in present-day America? Actually, I agree with you. It is offensive. But the fact that the comparison gives offense doesn't in itself make it incorrect. In fact, Dr. Hershaft wasn't the first to make this comparison. The first to do so was the great Jewish writer Isaac Bashevis Singer, winner of the 1978 Nobel Prize for Literature. Singer put these thoughts into the mind of one of his characters in his short story, "The Letter Writer":
"In his thoughts, Herman spoke a eulogy for the mouse who had shared a portion of her life with him and who, because of him, had left this earth. 'What do they know—all these scholars, all these philosophers, all the leaders of the world—about such as you. They have convinced themselves that man, the worst transgressor of all, is the crown of creation. All other creatures were created to provide him with food, pelts, to be tormented, exterminated. In relation to them, all people are Nazis; for the animals, it is an eternal Treblinka." 2
Singer himself narrowly escaped Treblinka, widely regarded as the second most important German wartime extermination center, where a total of 870,000 Jews were killed. 3 It hardly needs to be added that Singer was vegetarian. But why is it, I wonder, that we find the comparison of a slaughter house to an extermination camp so disturbing?
Is it because Treblinka was a place where humans were massacred like animals (in which case, why is it acceptable to massacre animals, but not humans?). Is it because it defiles the memory of the victims of
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the Holocaust to be compared to the innocent victims of today's slaughterhouses? Yet that is precisely what the death camps were: vast industrialized killings machines that treated people just like animals. If we minimize this, then we deny the horror and enormity of the Holocaust itself.
Or perhaps it is, as Dr. Hershaft suggests, the fact that it is all simply too close for comfort. While six million Jews were being systematically and brutally massacred by the Nazis during World War II, most of the world stood by silent. While eight billion farm animals are killed in the United States each year, most of us stand by, equally silent. 4
Perhaps that reaction is, in truth, the most painful of all reactions ... a twinge of conscience.
THE BEST OF THE BEST
I wanted to see the best, not the worst, that the world's meat industry could show me, so I went to a celebrated farm in southern Britain on a squally spring day. This is a very special farm, because the animals here are treated better than anywhere else in Britain, probably the world. Their meat is sold for high prices at the best shops in London. If you can't quite go vegetarian, but you care enough to avoid cruelly raised supermarket meat, this is the farm you buy it from.
So here we are, in our Wellington boots, walking and talking with Richard, one of the younger generation of farmers who try to produce their meat in a kinder and more ethical way. First, I want to raise the question of terminology.
"You describe your meat as 'high welfare,' " I say. "Is that the same as 'cruelty free'?"
"I suppose so," he answers. "It's terminology, isn't it? I think, all in all, our welfare standards are the highest in the country, if not in Europe, if not the world."
"So are you saying there's actually no cruelty involved at all in your method of meat production?"
"I think that would be tricky, wouldn't it? I don't think you possibly could say that, really. I mean, it depends what you mean by 'cruel,' doesn't it? What I'm seeking to do is to rear the animals much
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the same way as any one of our customers would do if they did it themselves. In other words, I don't think a customer would, if you gave them ten porkers, they wouldn't build a mini-factory farm with gridded floors, cut its tail off, medicate it, choose a growth promoter. They'd find an old coal shed or something and put some straw in it, and feed it scraps. That's what we're doing. That's a fascinating question. You remind me of a guy from BBC TV who asked much the same thing—he asked if animals have rights or not, and I think it's a difficult one, it's a long discussion, you need more than half an hour's continuous chat, and probably as long to think about it."
"But you must have thought about it."
"Not exactly in those terms. I think my farm is undoubtedly high welfare, and I agree with you that's not the same as cruelty-free. I mean, supposing you have a pig that doesn't want to get on the lorry. We will pick it up and carry it on. If you wanted to be utterly cruelty-free, I think you'd have to let it go, and hope that it wanted to go next week. So at the moment, I'll say we are definitely high welfare, but to say that we are absolutely cruelty-free, 100 percent, would be difficult."
"What about the rights argument? Do animals have rights?"
"You'd have to talk to a priest about that."
"I'm asking you. Do you think animals have rights?"
"I think they deserve respect and kindness, particularly if you're using them as a source of food. I think they do anyway, but particularly, I say particularly because in a way you're then using them, as opposed to living with them. It's not as if they're performing some other function, such as a guide dog."
"It could be said that what you're really doing is just being kinder to meat eaters, rather than being kinder to the animals. Because it avoids the unpleasant thought in their mind that the animal they're eating has suffered."
"I wish that thought was stronger in their mind in the first place," says Richard. "I mean, I actually think that thought doesn't lurk much in people's minds."
We stop talking, and tour the farm. The wind is bitterly piercing, and the driven rain is turning the chalky soil the same leaden gray as the sky. I am grateful for the shelter of the first farm building we are
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herded into; but I am not prepared for the sight that meets my eyes. It is dark, but in the gloom I can see three vast sows, confined by metal frames, their teats exposed and constantly available to the baby piglets that run and squeak as we enter. The sheer bulk of these sows is breathtaking, even majestic. But these are not just female pigs, they are mothers, too. In the narrow farrowing crates in which they lie imprisoned, they are all but denied access to their own babies. They cannot even turn round. I catch one of the sow's eyes, and I understand the particular distress she is experiencing. When we resume our conversation, I tackle him about this.
"I wanted to talk to you about some of the things we've seen today. Now the first thing that we saw was the farrowing crate, which has been criticized by various organizations. Can you tell us why it's been criticized?"
Suddenly, he has become very distant.
"I presume because it restricts the freedom of the sow. For the period of giving birth to the piglets."
"And what's your feeling about that?"
"I think if you don't, and the sow then treads on the piglets, or savages them, or they suffer in any other way, then it can create more problems than it solves. It remains a totally unsolved concept in this company. We allow all forms of farrowing, and both have advantages and disadvantages, and after six years we have no clear policy. And any honest welfare person wouldn't have, either."
"I must say I found it quite disturbing to see those sows like that. The first thing that hit me, when I went into the building to see those sows lying down, completely immobile, was what a common bond there is between the human animal and the pig animal. It seems to me that the meat trade is founded upon the exploitation of the female reproductive qualities of animals. Have you ever thought about that?"
"Well," he replies, "I think one of the saddest things in this country is that people are so far apart from all methods of production, and to anyone not used to keeping animals I'm sure it all seems terrible. I mean, those pigs are actually having a lot easier time than my own wife had during the birth of our children."
"Really?"
"Well, because they don't seem agitated, actually. I mean, they
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actually are not in the crates for very long, and they go in them very freely."
"But you are perverting natural maternal instincts, aren't you? Because you're confining that sow. You're stopping her from leading the full life of a mother, which all mothers, whether human or pigs, are entitled to. Surely that is a fundamental right?"
"I don't think so. Life is more complicated than that. That's too naive. That's dangerous stuff."
"What about veal. Isn't that inherently much more troubling? Killing a small, baby animal is surely one of the most horrible things that anyone can do. Doesn't that upset you?"
"Well, it upsets a lot of people, and I have to remind myself that it's similar to lamb. And objecting to killing a calf aged six months to a year is similar to killing lambs, which doesn't give me a problem, really."
"Why not?"
"If it's to die, and has lived a decent life, probably the length of time it's lived is irrelevant. It's a bit like one of the free-range chicken definitions, which actually gives a different echelon to an animal which has lived longer, in fact thirty days longer. I think that is absurd. I mean, you may accuse me of being an evil man for killing animals at all."
No, I don't think he's evil. After all, he has recognized some of the inherent cruelty in meat production, and is trying to do something about it. But I do think that he—in common with most farmers and butchers—hasn't thought through all the moral issues involved in the business.
"Your male cattle are castrated," I say. "Are you quite happy to do that?"
"As long as it's done with anesthetics."
"But essentially, it's still a mutilation."
"Yes, of course," he replies.
"But you think it's worth doing?"
"Well it doesn't actually harm the animal. I mean it depends what you call a mutilation. I've got a pierced ear; that's mutilation. I don't see it as a big problem. I mean it's part of keeping animals."
"How do they feel afterwards?"
"That would be an interesting research project. I've no idea."
"You've got no idea?"
"With beef animals, if you don't castrate them, you can't keep them outside. You're terribly stuck then. I would say that the choice between being able to get out in a field and the castration weighs in favor of letting it be outside, rather than keeping it in all the time. Very difficult decision."
Difficult, indeed. Now I want to raise another "difficult" issue, the question of human rights and animal rights. In common with many people of his generation, this young farmer was, at one stage, involved in antiapartheid demonstrations.
"Why do you feel that's an important issue?" I ask.
"Because there is discrimination in South Africa between two sorts of human beings, based entirely on color."
"So it's wrong to discriminate between the same species, on the grounds of color or genetic constitution, but it's OK to discriminate between species? That's OK?"
"I don't have a problem with it," he replies.
"What makes it all right?"
"I go back to the simple fundamental fact there is no moral problem, for me, with eating meat. It's every man's choice, and I'd love to spend hours arguing the philosophical point, and heaven knows, eventually one might be convinced. But my gut feeling tells me that eating meat's all right, as long as the animal's not abused."
"But surely," I reply, "there's no greater abuse than taking a life unnecessarily?"
"I mean during its life."
"So it's OK to commit the ultimate abuse—taking a life—but it's not alright to commit lesser abuses along the way?"
"I would say," he answers, "that living torture is probably worse than death. Isn't making an animal suffer during its life worse than killing?"
"I think it's better if the animal had never been born." I feel I have to push him now, to make him explain precisely how he justifies what he does. "But tell me, in your mind, is the pleasure you get from eating a lump of steak worth X amount of suffering to the animal?"
"That's what you call a loaded question."
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"No, it's not a loaded question. I'd like a clear answer."
"The clear answer is this, that I do not believe that the way we rear animals involves suffering during their lives. Nor even their death. So it doesn't suffer. So I'm not balancing the pleasure against the suffering, I am balancing it against the life of an animal. And I square that simply because I do not see the eating of meat, and therefore the killing of an animal that has lived properly, as fundamentally wrong. And that's where you and I differ."
"The only difference is that I view the taking of a life as murder," I say. "But you don't, do you?"
"Not of animals. Do you?"
"Yes, of course."
There is an iciness in the air now.
"Are you prepared to do violence about it?" he asks me. His eyes have narrowed, and his lips are pursed. His question takes me aback.
"What do you mean?"
"I mean," he says, "there are those who burn lorries and blow people up because of it. What about that? You answer that, you owe me that much."
"Of course not," I say.
We stop talking.
THE SCIENTIST
I'd first met Dr. Alan Long at the Vegetarian Society. One of the most renowned organic chemists of his generation, he is not the kind of person to take an overly sentimental view of animals. I went to talk to him.
"Are you an animal lover?" I ask.
"I wouldn't call myself a great animal lover," he says. "I'm a great respecter of animals, and I think that when they die, they're entitled to be treated with respect, just as when human beings die."
And Dr. Long certainly knows about death, and how it comes to our food animals. For several decades, he has visited livestock markets and slaughterhouses, witnessed and recorded events there, and used this information to become one of the most informed and respected critics of our process of meat production.
"What made you get involved in this area?"
"My mother was involved with a campaign in the 1930s to abolish the pole-axe," he says. "Because of that, there was always an interest in animal matters in my family. I was very much influenced by the parable of the Good Shepherd, and I couldn't equate the allegory with the dead lamb on my plate. I decided that I preferred to see lambs in fields rather than mutton on the dinner plate. My parents were understanding, and said, 'All right, you don't have to eat lamb if you don't want to,' and so we thought it through, and gradually all of us became vegetarian.
"My mother was still concerned with animal welfare, and I went to see livestock markets with her. I suppose I was an inquiring little boy, and I asked more and more questions and eventually decided that something ought to be done about the things I saw.
"So I started to collect facts, and I became a campaigner for what was then generally perceived as a really nutty cause. I decided that the best way of dealing with this perception was to get the facts, and use them in an unemotional way."
"Now, your scientific background is quite significant, because many within the meat trade and the farming industry accuse people who feel concerned about the plight of food animals of being over-emotional. "
"Yes, I thought that the animals should speak for themselves. And I don't believe in accumulating facts without making them work. I don't believe in collecting facts like stamps, just to look at and admire. I was, if you like, a self-appointed shop steward for the animals, constantly putting out all the facts I could uncover."
"Some farmers have said to me that the animals in their care are really quite happy for most of their lives, and that people like you and me are just being over emotional. How do you react to that? "
"I would say that they have no real grounds to make that assertion; in fact, they're being emotional by saying that. You have to ask, 'How do they know? Where is their evidence?' On the other hand, we certainly have scientific evidence that many animals suffer very considerably—you can do lots of experiments on stressor hormones, you can look at dehydration, that sort of thing. And I think that many farmers would privately agree that animals sent to market suffer very greatly."
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"But when a farmer says to you, 'prove that my animals suffer pain/ what would you say to him?"
"Well, a lot of work has been done on this. The first thing you can point to is the general condition of the animal: many of them look quite poorly, their coat isn't in good order, that sort of thing. Then there's the environment—they suffer from the cold and the wet, just as we do. You can see cows in hot weather that are so thirsty that they try to lick the urine off the concrete, and that to my mind is definitely a sign that they are suffering. You can analyze the concentration of stressor hormones, the concentration of sugar levels in blood—all of these are signs of stress. There are 30 cases of mastitis for every 100 cows in a dairy herd. Mastitis is an inflammation. It doesn't take much imagination to think that an animal doesn't like mastitis any more than a human being does—inflammations hurt. Lameness is another prevalent problem. And you can survey the health of animals arriving at the slaughterhouse. One study has shown that 30 percent of all chickens have sustained broken bones being transported to slaughter. There's a dumpster at one market I visit where they throw the bodies of pigs that have actually died on their way to market. This sort of evidence is really incontestable."
"Pigs are particularly susceptible?"
"Yes. With modern breeding, you can see that they have been bred to be fleshy—they're really travesties, these animals. And that puts a strain on their hearts, because their organs haven't been adapted to meet the demands of intensification; they are ill-equipped to deal with the effects of stress."
"But farmers say that it's in their own commercial interests to keep the animals happy, otherwise they don't put on weight, or produce enough eggs."
"That's an old, discredited argument. Of course, they do put on weight—unhappy people will put on weight. Unfortunately, cows will continue to give milk, even though they're in a very bad way. This is understandable, because Nature's way of survival is that certain processes will go on, right to the end. The other point you have to remember is that these animals don't have to live very long. Nearly all the animals that are in production in this country are killed off in one way or another before they reach puberty. Sadly, what farmers do
instead of looking after their animals with 'tender loving care' is to shovel in loads of drugs to keep them going—growth boosters and that sort of thing."
"Tell me about your first slaughterhouse experiences. "
"Well, the first I went into was a little poky place. To some extent, I'd been prepared for it, because my mother had been into slaughterhouses, of course, and she'd told me. She didn't encourage me to go in, but when I was a big boy, and ready for the facts of life and death, I went in. And I was horrified, and I am still horrified. They were slaughtering horses. They weren't stunning them first; they were just cutting their throats."
"How on earth can you cut a horse's throat without somehow immobilizing it?"
"They hoist it up by its back legs."
"So you've got this enormous horse, just struggling on the end of a chain?"
"Yes. You will see an animal in that sort of circumstance, struggling about for a minute or so, rather like a huge, wriggling puppy."
"Now, people say small slaughterhouses are better?"
"Well, that varies a great deal. Today, most slaughterhouses are very large; they're essentially killing factories. You can go to a slaughterhouse where they're killing chickens, and the enormity of the whole scale is really quite appalling. These chickens being shackled upside down on conveyor belts, and being mechanically eviscerated, and mechanically defeathered. The sheer scale of the massacre—which is what it is—is rather horrifying. And the whole smell and stench of death pervades the place. The trouble with a killing factory is, if anything does go wrong, then it can go very wrong indeed."
"You've actually seen religious slaughter, which very few people have. What happens?"
"At the first one I went to, the foreman said to me, 'I can tell that you find this horrifying—I do too.' Well, he was an honest man, I suppose. The Jewish law requires that you use a very big knife to cut the throat, and in one stroke. In order to do this ritual, the animal has to be prevented from struggling about too much. The biggest problem that presents itself with large animals is to get them down. So in the early days, they used to tie the animal, hobble it, and throw it on the