Lethal Legacy: BSE – The Search for Truth 
by Stephen Dealler.
Bloomsbury, 307 pp., £5.99, April 1996, 9780747529408
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BSE: The Facts 
by Brian Ford.
Corgi, 208 pp., £4.99, May 1996, 0 552 14530 0
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Agriculture and Health Committees. Bovine Spongiform Encephalopathy (BSE) and Creutzfeldt-Jakob Disease (CJD): Recent Developments 
HMSO, 149 pp., £17, May 1996, 0 10 237796 0Show More
Beyond Beef: The Rise and Fall of the Cattle Culture 
by Jeremy Rifkin.
Thorsons, 353 pp., £8.99, June 1996, 0 7225 2979 1
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All flesh is grass, said Peter the Apostle. In the United States, a calf runs the range for less than a year before going to a crowded feed-lot. It is treated with hormones to promote weight gain. Both there and in Britain the beast is likely to be drenched with antibiotics to keep down diseases and to promote further weight gain. It has one role in its short life – to get fat, on corn, sorghum, wheat, soybeans, whatever. This stuff is saturated with herbicides and pesticides. Consumers pay for what they eat: the National Research Council of the Academy of Sciences estimates that beef pesticide contamination represents 11 per cent of the total cancer risk from pesticides in US foods. On the other hand, the quicker you fatten a beast for slaughter, the higher your return.

Dairymen in the US or Britain have to think along the same lines. Are you going to leave the cow to eat grass (including hay and silage) all year round? How much milk will that yield? And how many cows can you stock that way? It pays to buy in feed – providing it is cheap enough – and get either more per acre or more per cow or both. If you want a twice-daily Niagara of milk and cream as output, you have to do some lateral thinking about input. A cow is a ruminant with a complicated stomach arrangement, wonderfully adapted to convert grass to protein. Left to itself at pasture, it would calve, nurse, wean and dry up. But a cow is not left to itself. It has a calf and then swiftly says goodbye to it, but twice daily milking keeps the hormone system producing as if the calf were still there. Milk is complicated stuff, protein from vitamins and cellulose via a two-stomach process. A short cut is to deliver protein directly into the digestive system.

Any animal that eats grass also consumes a significant proportion of animal protein with it: snails, slugs, worms, larvae, even winged and wingless insects. For all species but one, vegetarian diet is an adaptation, not a moral position. Those inadvertent savoury snacks are probably welcome. Wild bovids must originally have roamed the plains, steppes, savannahs and prairies following grass and anything else they could find. Domestic bovids cannot migrate, so the anything else arrives by other means: dried grass, fermented grass, and cattle cake or pellets, high in protein. Milk for months, or steak marbled with fat, requires cheap protein. Any biological material will serve as a starting point. In the US, according to Jeremy Rifkin’s new book, some feedlots have been experimenting with cardboard, newspaper and sawdust. Others have been scraping up manure from pigpens and chicken houses and adding it to the cattlefeed. The stuff contains nitrogen and other minerals, so why not? What is food? A mixture of hydrogen and carbon and a few other elements available in solution, in long complicated chains: oil fits the description, and so does industrial sewage, so those, too, might go into the porridge. Why should cattle be deprived of a calcium supplement? Cement dust, which is an oxide of calcium, may be just the thing: the US Department of Agriculture says a shovelful of cement dust in the trough produces a 30 per cent faster weight gain.

There is a problem about delivering all this supercharged supplement to a beast with a digestive tract designed by evolution to take tiny amounts of nourishment from huge volumes of sere stuff like grass. The civilisation that invented All Bran understands this problem perfectly. Cows, too, need roughage. (Indeed, cows, unlike humans, have evolved to do very well almost entirely on roughage.) So scientists at Kansas State University have been working on artificial roughage in the form of little pellets of plastic: 80 per cent ethylene maybe, and 20 per cent propylene. It is cheaper than hay. And after you have slaughtered the animal you can scrape out maybe 20lbs of the stuff from the rumen, melt it down and recycle it. But what comes out of the cow’s back end is not the main concern here. What is of concern to cows, farmers and public is what goes in to make the milk. In Britain, for decades – indeed since before the war, says the Ministry of Agriculture, Fisheries and Food – farmers have been buying, as part of cattle food mixture, a crunchy, lightly toasted, dried food snack packed with all the minerals and proteins a body might need to survive. It is, of course, baked meat and bone meal made from the carcasses of dead ruminant beasts, such as cows and sheep. You could think of it as grass in concentrated form. In the interests of cheap food bovids with naturally coarse vegetarian tastes have been persuaded to turn not just to carnivory, but to a tasty form of cannibalism as well. Man interferes with nature, and nature strikes back.

Bovine spongiform encephalopathy was identified in a dairy herd of Holsteins in Kent in November 1986. The implication is that until then it did not exist. Some members of the British Veterinary Association have never been sure of this. Some of them think it might always have been around, a very rare, random affliction, dramatically amplified when a demented beast was turned into crisps and fed to its relatives. Another working hypothesis is that it ‘crossed a species boundary’: scrapie, known to exist in sheep for the last two hundred years or more, survived the process of converting a sheep into food for Holstein dairy cattle. Like BSE, scrapie is a spongiform encephalopathy. No human has ever been known to catch it. On the other hand, there is, and has been for many decades, and in more than one form, a human spongiform encephalopathy. It is signalled by unsteadiness, loss of control and memory, and dementia, and it ends wretchedly, but the condition is not normally diagnosed with certainty until after death. On examination, the brain is marked by holes, like a sponge.

One form of this illness is called Creutzfeldt-Jakob Disease or CJD. Some people seem to inherit a risk of it: about 10 per cent of cases are hereditary. (There is a very rare form known as Gerstmann-Straussler-Schenker Syndrome or Fatal Familial Insomnia.) Others get CJD for no discernible reason. A tiny, tragic group of people are believed to have contracted it after taking growth hormones extracted from the pituitary glands of human cadavers. There is another form, endemic in a tribe in New Guinea: it, too, is a spongiform encephalopathy, called kuru or the laughing disease. The tribe honoured its dead by eating or otherwise ritually handling their brains. This practice has ceased, and the disease is dying out, but for a while it was well studied. CJD, by now, is also well-studied. It is a rare disease, occurring at a rate of rather less than one case per million per year. It has been occurring at this rate in Britain for years, both before and since the start of the BSE epidemic, and in Israel and Austria, where there is no BSE, and in India, where they don’t eat beef and cows are sacred. One case in a million per year is truly rare; it is the prospect of a future sharp increase which has caused alarm. CJD is a disease for which there is no explanation and no known treatment.

It is important not to get CJD out of proportion. It is one of a suite of neurodegenerative diseases in which things go wrong with the central nervous system, or the spinal cord, or the brain itself: these things happen in motor neurone disease, multiple sclerosis, Parkinson’s disease, Alzheimer’s disease, or even strokes. Nobody knows why they happen, and nobody knows how to halt or even satisfactorily slow the degeneration. Robert Will, the neurologist at Western General Hospital in Edinburgh who heads the Government’s CJD surveillance unit, points out that although CJD is rare, we still know a great deal more about it than about many other more common neurological diseases. There are, however, some important questions concerning BSE and CJD to which there are not yet answers. Nobody knows – there are theories but no facts – how BSE is transmitted. If there is an agent of either disease, no one knows what it is. To simplify wildly: there is a proposal called the prion hypothesis, which posits a rogue protein suddenly instructing its neighbour proteins to go maverick too. Because it replicates itself, it is a form of life, but not one based on the nucleic acids that make up DNA, which is, as far as we know, the basis of all life on Earth. There is an alternative hypothesis, for which there is not much evidence either, which is that the agent of the disease might be a ‘slow’ virus. There are such things, and they are immensely difficult to detect. A number of cancers are believed to be spread virally, but nobody knows why, or how.

The other thing nobody knows for sure is why or how BSE got into the cattle population. Suspicion at the start focused on cattlefeed based on meat and bone meal from other ruminants. That was because it did not occur in herds fed entirely on grass, and there didn’t seem to be any other common denominator. There was even a plausible explanation for why BSE began in 1986: in the very early Eighties, the British rendering industry changed the process by which a dead cow was rendered down to tallow, gelatin, hide, bone meal and hoof and horn for garden fertiliser; and at the same time, more British farmers bought cattlefeed that contained ‘products of animal origin’ – a phrase which describes chicken shit, fishmeal or dead cow. Farmers changed their buying habits because prices for other sources of feed went up; and there was a glut of animal material so prices for that went down; and dairy farmers were having a hard time anyway so there was pressure to save on inputs while increasing outputs.

A number of reasons have been put forward to explain why renderers changed their practice, all of them true to some degree. One version has it that the rendering industry stopped treating the carcasses with chemical solvents to extract the fat because it was dangerous for their employees. Another, advanced by Brian Ford in The Facts, is that nobody wanted the fat any more. Another is that the workload required a more efficient way of processing carcasses – a kind of continuous disassembly line, rather than processing a ‘batch’ at a time. Labour Party spokesmen have been pointing out that proposals drafted by Labour in 1978 to tighten processing practices relating to cattlefeed were abandoned after the 1979 election because the ideology of Thatcherism held that industry regulated itself better than government could regulate it.

Whatever the reasons, the routines were altered. Carcasses were no longer treated with a powerful solvent, and when they were ‘cooked’ to drive off all the moisture and kill pathogens, the material was exposed to a lower heat for a shorter period. Whatever the agent that might cause BSE, the reasoning went, it had been destroyed by the old process but was not destroyed by the new one. You don’t have to know much about biology to reflect that the agent of BSE must be a very peculiar thing. You can’t destroy it by cooking or sterilising or pasteurising or freezing or drying it. By implication, it also survives assault by salivary and gastric enzymes in the normal digestive process and passage through the gut and somehow gets into, and makes its home in, the central nervous system, and in particular the brain, where it then instructs your own personal proteins – the ones that define your identity, the you within – to go bananas. But nobody knows how it sets about its dreadful work, or in what concentrations it must exist before it has the oomph to overcome the amazing natural defence systems that living creatures have against infection.

The classical CJD of humans is a disease of the elderly, almost unheard of in the under-65s. It steals up slowly to take a life away. The transmissible spongiform encephalopathy is like something out of science fiction: The Invasion of the Body Snatchers keeps coming to mind, except that there are no pods and – until March 1996 – there were no discernible human victims. There were, however, more than 150,000 cows in 35,000 British herds dead, or staggering wretchedly towards death.

When BSE first appeared in Britain, and began spreading among the dairy herd, there were two sets of reactions. One set came from a small number of vets, microbiologists and public health officials, who said: this is something to worry about. This reaction was countered by a larger group of ministry officials, chief medical officers, other vets and animal scientists, and above all ministers themselves, who chorused, like the wicked baron’s bailiffs in a pantomime: oh no, it isn’t. The ministry men argued that BSE was like scrapie, and scrapie had never infected a human, and eating meat from animals that might have carried the disease certainly couldn’t give anybody CJD, because CJD was very rare, wasn’t infectious, and anyway existed before BSE. This, however, was a ridiculous position, because the scrapie theory also implied that the spongiform encephalopathy had crossed a species boundary: if from sheep to cow, why not to human? This official position – that there was nothing to fear – was made even more ridiculous when in 1988 the Government banned the use of ruminant-based proteins in feed for cattle (but not for pigs, or chickens): why would they ban it if there really was nothing to fear? The public took the hint, and began to waver in its passion for beef, and especially beefburgers, which, of course, include bits of dead cow you’d just as soon not know about. Ministers went on making soothing statements. The Agriculture Secretary, then John Gummer, notoriously fed his daughter a beefburger on television. It became clear, too, that in some way officialdom was leaning on the vets and scientists in officialdom’s pay, telling them to damp down their cries of alarm. ‘They didn’t seem to want publicity with the disease,’ one vet said in 1989. ‘It did seem to me a little odd that we were asked to keep somewhat quiet.’

Questions remained unanswered. What infection? What victims? What proofs? What agents? What environments for hazard? To scientists the words ‘We don’t know’ are not admissions of helplessness but starting-points. Science is the art of setting ‘don’t know’ to work. The first scientists confronted smallpox before anyone knew about viruses, and controlled tuberculosis with antibiotics before they knew how antibiotics worked, or what the bacillus actually did. They couldn’t see the agent, but they could certainly see the threat.‘We don’t know’ is also, in some ways, comforting: we don’t know to what extent the risk of CJD is involved in eating beef, and there might be no risk at all, but whatever it is or is not, it pales beside those we do know about: smoking cigarettes, or drinking alcohol, or driving a car or riding a bicycle. Or, for that matter, the risk of heart disease from regularly eating rare beef, or cancer from overcooked steak. So then, and even now, there are scientists who look troubled when you talk about the ‘dangers’ to humans of eating beef. What, they ask, are these dangers, actually? And, meanwhile, what about the farmers on whom all the economies of the world depend? How can we tell you not to eat their products? How do we answer questions like that? So much for trying to see it from officialdom’s point of view. Having banned the use of ruminant tissue in ruminant feed in 1988, the Government then proceeded in 1990, a year after the petfood manufacturers had already done so, to specify which bovine offals might no longer be used as food for humans – eyes, brain, spinal cord, thymus, tonsils, spleen and intestine. This was another signal that confused the consumer. If British meat was perfectly safe, and if BSE could not cross the species barrier, then why ban the offal?

Once, while writing a hasty story-so-far about BSE as a background to some other twist in the saga, I suggested that the Government itself showed all the symptoms of mad cow disease: it staggered from one policy to another, striking demented attitudes and producing nothing of value. It seemed like a cheap shot at the time. What has happened since has made it seem a bit less cheap. When you talk to senior vets and scientists from the tier called upon to advise the Government, you come away with a sense of their exasperation and contempt. Briefly, the BSE story teetered about for most of this decade, provoking low levels of alarm, as the number of cases failed to fall sufficiently swiftly, and as yet more animals – including zoo creatures, such as kudu, oryx, ocelot, elk and puma, fed on suspect supplements, went down with the disease. The notion that BSE was not ‘transmissible’ began to look very silly. Agencies established by the Government – the CJD surveillance unit, the spongiform encephalopathy advisory committee and so on – said things that were, from their point of view, true: yes, the BSE epidemic ought to be on the way out; no, the risk of contracting CJD from eating British beef was never more than very slight, and no, there was no evidence that those most at risk were going down with BSE. If there was a link between CJD and BSE, you’d see it first in abattoir workers, who actually cut up spinal tissue with chainsaws, and who smashed skulls, spattering themselves with the stuff, breathing in fine aerosols of infective meat and gristle, blood, bone, skin and nerve. After that, you’d expect to see it in farmers and farmworkers. Actually, what evidence there was – remember, hardly any evidence at all – showed that ministers of religion were more likely to end up with CJD than farmers.

By November 1995 official complacency had begun to falter. First, there were the figures for the 1994 deaths from CJD, which had risen on previous years. And then the British Medical Journal published a series of papers on BSE and the human link, and in particular, the probability of the deaths of four farmworkers being more than coincidence. Education authorities started erasing beef from school menus, and ministers once again started telling the nation that beef was safe. In fact, there were already rumours that all was not well, and stories circulated of young people with CJD. Late in the year the likely tally for 1995 deaths became known. It was well down. You can’t have an epidemic without bodies: the alarm subsided again. Ministers went on saying what they had always said: that the best scientific advice assured them that all was well, and they were acting on it, as they always had, to remove even the teensiest scintilla of uncertainty. It was just the Government’s bad luck that, shortly afterwards, in National Science Week of all weeks, the Secretaries of State for Health and for Agriculture met with members of the spongiform encephalopathy advisory committee, now chaired by John Pattison, Dean of University College London Medical School, who told a different story. There had, in the previous year or two, been ten cases of CJD quite unlike classical CJD, with different symptoms and a different kind of progress, but the same tragic outcome. The pattern of holes in the brain tissue after death looked much more like BSE (or the kuru observed in New Guinea cannibals) than classical CJD, and the victims were all alarmingly young. Scientists were no longer prepared to conspire in the story that there was no conceivable link between BSE and CJD.

They don’t, however – they didn’t then and they don’t now – claim a link has been proven. But there was the sound of chickens coming home to roost. People like Stephen Dealler, a microbiologist at Burnley General Hospital, had been pointing out publicly for most of the Nineties that there was always a solid chance that a spongiform encephalopathy was transmissible, so it should always have been assumed that humans could catch it. More to the point, BSE was mostly in the dairy herd because dairy cattle had longer lives than beef cattle. But beef cattle sent for slaughter may have had the disease although not (by then) the symptoms. So the British might have been dining on infected tissue for years. The logic was there, and nobody on that day seemed prepared to challenge it. We might all be infected, we might all go mad and die. Scientists could say – and they do say it, over and over again – that they cannot demonstrate infectivity in the muscle or red meat of cattle, nor in their milk. But the damage was done. The hamburger we fried for supper, the milk we drank in our tea, the gelatin round the cod liver oil capsule we took at breakfast, might all contain the agent of a transmissible encephalopathy, this terrible, invisible, indetectable little thing that might enter our brains, and alter our identities.

Within a few weeks, the British Government had somehow managed to turn the issue inside out. What was a humiliation for Westminster, a disaster for the farming industry, a calamity for the meat trades and a tragedy for up to a dozen families somehow became – with the enthusiastic connivance of most of the British press – a story of plucky little Britain taking on the brutal bureaucrats of Brussels and the greedy, advantage-seeking ministers from Bonn and Paris who supported them in their decision not to allow the export of perfectly safe British beef, never mind British bull semen, tallow and gelatin. How this was done will make an instructive essay in spin-doctoring and bad government. A number of things have become quite clear. One of them is that the Government seems not to have taken BSE in British beef seriously until Brussels did. Mr Major and his ministers have repeatedly talked of getting ‘the best scientific advice’ and of ‘doing what our scientists tell us’ (which included entertaining – for a day or two – the idea of slaughtering the whole UK herd).

The Government’s pious invocation of science has its comic side. Between 1986, when BSE first appeared, and 1996, when the Government finally accepted there was a problem, the Ministry of Agriculture cut its research budget by 25 percent in real terms. It also sacked around 1800 scientists and technicians. It is still talking airily of selling off important government research institutions, such as the Institute for Animal Health. Who would it sell to? Animal feed manufacturers? The German beef industry? McDonald’s? The Government did indeed ban the use of ruminant material in ruminant feed in 1988: there is no evidence that much attention was paid to policing the ban, or to withdrawing the stuff already out there. The old bits of dead sheep and cow were mixed to feed poultry and pigs. And then, the feed manufacturers mixed up the newer, safer recipe for cattle in the same hoppers, which meant that it was probably still contaminated with the old BSE agent. This is quite clear. There is a kind of cow known as a BAB: born after the ban. BABs now account for 60 per cent of all cases. Some of them – it transpired after lengthy research in August – might have been born of infected cows: another nasty surprise for some experts, who had been convinced that there was no ‘vertical transmission’ from cow to calf. ‘If you take that in conjunction with the fact that we are still recording 200-300 cases of BSE a week,’ John Pattison has said, ‘I think it begins to show some of the weaknesses of the UK situation when discussing with colleagues abroad the possibility that we have everything under control.’

And then there is the matter of the specified bovine offals: the bits of eyes, spleen, thymus, spinal cord, brain and so on that must be removed before the meat from a slaughtered animal goes into the food chain. This ban was imposed in 1990. There are 12 million cows and bullocks in Britain. Slaughtering is a good, steady job. It wasn’t made clear at the time how a slaughterman was going to use his chainsaw to remove the dangerous stuff yet leave the best cuts untainted with the suspect organs, and it is now clear that he didn’t try too hard. The Agriculture Secretary Douglas Hogg revealed to the House, and later to a Parliamentary committee, that of 193 visits to slaughterhouses, ‘failings’ in the handling of bovine offal were found in 92. Helpfully, he added, he had called in the industry on two occasions ‘in the latter part of last year’ to make it plain ‘how important it was to achieve the full implementation of the regulations’. It could not be plainer. Five years after the imposition of a ban, the Government told the slaughterhouses that they really should start thinking about implementing it properly. Then there is the interesting matter of what happened to all that animal feed that didn’t get fed to British cows. It is now known that a lot of it was ‘dumped’ in France, where French farmers snapped it up. Some of it might even have been bagged again and exported back to Britain. European legislation requires feed to be labelled as containing ‘products of animal origin’. Who is to know? One of the 12 sufferers of the new variant of CJD is French. Remember all this when you hear a British politician talking about the Europeans being unreasonable.

Earlier this year, French scientists, together with a member of Britain’s CJD surveillance unit, reported in Nature that they had injected stuff from the brains of mad cows into the skulls of macaque monkeys, and sent them mad too. The monkeys experienced variously edginess, depression, voracious appetite, intermittent priapism, ataxia, myoclonic jerks and so on. Their brains after death showed lesions, sometimes grouped into small clusters, indistinguishable from the new form of CJD. This experiment doesn’t answer all that many questions – certainly not about how you might actually get CJD from eating a bit of mad cow – but it does support the hypothesis that BSE is now in the human population. It provides no answers as to whether some people are more at risk than others, or whether those who eat beefburgers are in greater danger than those who eat filet mignon.

‘An awful lot is known about Creutzfeldt-Jakob Disease, a huge amount about the clinical features, the pathology and the epidemiology of this condition,’ says Robert Will. ‘However, there remain uncertainties about the nature of the agent. There is a huge amount of work going on and a lot of advances are being made very quickly in this field. We may understand much more about what happens at the cellular level in the next few years, and that is very important, because it might, theoretically, lead to some form of treatment.’ It isn’t the only question that will be answered in the next few years. The problem is that CJD is likely to be a long-incubation disease, which means that if the new variant is indeed transmitted by an agent in infected British meat, then the number of sufferers could rise starkly, and keep rising for a decade or so. Right now, on paper, you are still more likely to win the big one on the national lottery than contract CJD. Fifty or so cases a year is not a lot. Today, you are ten times more likely to get motor neurone disease than CJD. You are 100 times more likely to die in a car accident and a thousand times more likely to die of cancer. That’s the way it is now. The future could be different. BSE and CJD are likely to remain burning issues for some time to come.

Cows – their legs pointing crazily into the air as the flames lick round them – are burned on funeral pyres on farms only when the disease they have – foot-and-mouth is the most notorious – is so infectious that it would be dangerous to move the carcasses. The Government has a number of slaughter policies designed to control the disease or maybe just placate the Europeans. (The British Veterinary Association spokesmen, who don’t approve the killing of healthy animals just to show you are doing something, talk disdainfully of the Government ‘pulling slaughter policies out of hats like rabbits’.) Cows that actually develop BSE will have to be destroyed in special incinerators, popped in whole, and roasted at 850°C, to destroy all the protein. Cows that don’t will no longer be recycled into meat and bone meal for animal feed or garden fertiliser – at least while the disease runs its course. They, too, when they have reached the end of their useful lives, will be burned. The latest idea is to burn them in power stations. You can’t, of course, just shovel whole cows into the furnace, so the cows will have to be dismantled first. This will be done by rendering. The cow will be cooked at 140°C or so to remove all the liquids: what comes out at the other end, the experts say, will look a bit like demerara sugar. Then the rendered cow will be ready for shipment as fuel to a power station. In fact, the first stage of the experiment began in July. About a hundred tons of meat and bone meal were tested in a Rechem chemical waste incinerator at Hythe in Hampshire. But if cows are burned as fuel, they’ll go into the furnace by the shovelful at temperatures of 1000°C, at the end of which, there will be no protein left, only a fine fly ash. The metaphorical possibilities keep popping up. Hundreds of thousands of cows will have to be consumed by flames, not by people. After all, nutritionists regard food as fuel – calories measure heat output as much as food input. It is a rather odd fate, all the same, for so much flesh which began as grass to end as ashes.

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Vol. 18 No. 19 · 3 October 1996

Tim Radford’s discussion of the BSE fiasco (LRB, 5 September) fails to mention the considerable and growing school of thought which sees organophosphorous (OP) genetic poisoning as the true cause of BSE and new CJD alike. Their common pathology (similar patterns of plaques of rogue prions) clearly suggests a common origin, but on the other hand does not offer the least support to the causative connections which the scientists involved initially snatched at. Only a common vector is indicated.

The infective feed theory, on the contrary, requires BSE to cause new CJD by a magic prion action converting healthy tissue to a cancerous variety. This relative absurdity from a scientific point of view results from the need to find the vector in feed which has been rendered or cooked. Hormones do not survive heat treatment, so of course they are not found in the feed. Some end proteins – a far more robust and stable variety – do; so the prions survive.

Thus is the magic prion born! As sole survivor of cooking and rendering it must be infective. But infection is by live cellular microorganisms, bacteria, fungi or viruses; not just by molecules, however complex. You do not expect to catch a brain cancer from the patient in the next bed. Hormones and enzymes are giant organic molecules with thousands of radicals and can respectively trigger or modify protein formation. Not everybody knows that some 80 per cent of the human genome is otiose and unexpressed. Much of it is shared with our fellow mammals, a museum of evolution, and can still be expressed if the hormone to trigger it comes along. This is how we come to share with our bovine cousins the same rogue sectors of DNA which can be triggered into production of rogue protein. It is clear the common vector is a hormone mimic.

All the laboratory tests of brain tissue injection into animals merely confirm that hormones (uncooked) do the trick if the DNA is present. But since the hormones are not present in cooked/rendered feed these laboratory tests destroy the credibility of this Ministry of Agriculture, Fisheries and Food magic prion infective feed idea. The chances of a hormone reforming after being broken down by heat are as likely as the classic case of a Flying Fortress being reassembled by a hurricane blowing through a scrap heap in the Mojave Desert. Who, other than MAFF, would want to fly such a kite?

Organophosphorous insecticides contain the same nerve gas agents that Saddam Hussein used on the Kurds. In a thoroughly misjudged bid to be the first in the EC to eradicate the warble fly from the national herd, the Ministry of Agriculture authorised and indeed required the douching of cows at four times the strength thought safe anywhere else in the world. The warble fly campaign was a success: unfortunately it has eradicated far too many of the national herd as well.

The OP has phosphate radicals identical to the phosphate radicals composing the side chains of DNA, enabling them to exchange; thus breaking into the DNA chain and exposing the rungs of peptides on the inside so that RNA forms on the exposed sectors and then goes on to assemble amino-acid chains (proteins) in the cell, mediated by enzymatic catalysis. This is the hormone function exactly, so the OP can be described as a hormone mimic triggering rogue protein formation.

There are over six hundred officially recorded cases of brain damage in farmers caused by the use of OP insecticides on MAFF files, dating back to the beginning of their use for dipping sheep. But MAFF blames farmers for not covering themselves adequately and accepts no responsibility, although they have never addressed the question of inhalation, a rather bizarre omission when dealing with a nerve gas.

The only other countries to have used OPs for warble fly douching of cows were Eire and Switzerland; and they are also the only two countries other than Britain to have had cases of indigenous BSE recorded. They have had about two hundred cases apiece, with OP used at a quarter the strength used in the UK, compared with 167,000 cases in this country. In a rational society that would terminate the debate. In Northern Ireland full-strength douching was introduced three years after the rest of the UK; and BSE cases have followed the UK pattern, three years later. The feed exported to France after the ban in the UK was pig food, not cattle feed. There are no French (or other) cases of spongiform encephalitis in pigs.

The accusations of failure to comply with or enforce the regulations were presented to explain the mismatch between feed theory and the epidemiology. So were the supposed cover-ups in the EU. The long incubation was derived from a similar predicament; it is otherwise unevidenced.

Dairymen lost a month’s milk cheque if they used insecticide douches other than OP, because OP was thought not to infect milk. Beef farmers with no milk cheque to lose mostly avoided OP because of its poisonous record with sheep dipping. That is why over 80 per cent of BSE is in dairy herds. MAFF has tried to argue it is because dairy herds got more feed. But they have been forced to argue at the same time that a single gram of infective feed is sufficient to trigger BSE – the weight of offal in feed (the brains mostly went to France where cows’ brains are a delicacy, but they have not had any increased BSE as a result) was otherwise insufficient to have triggered the cases which have occurred. It is rather unscientific to try and have it both ways.

In the same edition of the LRB the immediately following review by Anthony Giddens of the Colborn-Dumanoski-Myers book on organic polymer pollution of the environment is entirely relevant to all this. Unfortunately, ecological arguments against runaway pharmaceutical innovation can be ridiculed as the musings of pinkies with bees in their bonnets. After all, science, mediated by the international conglomerates, is beneficial and progressive.

The truth is that some is, but some, when errors are made, can land us all in disaster. This is what happens when mistakes by officialdom are covered up and science is distorted for the purpose: you end up having to accept one excess after another to continue the false line of reasoning first introduced. When you add the confrontation between technologists with commercial tenure and those with academic tenure (at half the pay), you have the makings of a fiasco.

Merton, Norfolk

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