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CJD, BSE and Foot and Mouth: Who or What is to Blame?
Can These 'Experts' be Trusted with our Health?
Over the past two decades we have been subjected to a food scares to such an extent that we are left wondering what food, if any, is really safe to eat. We've had salmonella in eggs and poultry, BSE in cattle, pesticides on vegetables and fruits, genetically modified foods and now, foot and mouth in sheep and pigs. What has gone wrong? Who or what is to blame?
Crutzfeldt-Jakob Disease and BSE: Is there really a connection?
With all the recent publicity, you might think that we have a high incidence of
Creutzfeldt-Jakob
disease (CJD) in Britain, and that this in turn is caused by BSE, the so-called
'mad cow disease'.
Government tells us beef is safe but scientists bicker and we don't believe
them.. Confused and
frightened, particularly for our children, we shun beef, one of our most
valuable foods. In 1995
many County Councils voted to stop buying beef for school meals. We cannot
blame parents for
their reaction in view of all the publicity. But these were decisions made
solely on a gut reaction,
without knowing the facts.
The experts didn't help. Professor Richard Lacey,
the
microbiologist who started the scare, said on television in December 1995 that
he ruled out
scrapie in sheep as a cause of BSE but that CJD must have come from BSE
'because it had to
come from somewhere and BSE was the only place it could have come from'.
(1)
This is not only
quite illogical, it is also demonstrably untrue. He alluded to two recent cases
of CJD in children,
which were worrying, he said, because they were the first. No they weren't:
there have been
scores of cases of CJD in children as young as 10 over several decades, all
well documented in
the medical journals. That's the reason why the use of human growth hormone
from cadavers was stopped.
The fact is that CJD is an extremely rare disease with an average frequency in humans worldwide of less than one case per million per year. (2) It is one of seven similar diseases which affect many animal species and is endemic throughout the world.
The first case of CJD was identified in the German Backer family way back in 1920; (3) the first case of BSE in cattle was not until 1985. (4)
If eating cattle with BSE did cause CJD in humans, then we could expect more cases in countries with BSE than in those without it. And we could also expect more cases since the outbreak of BSE than before it. But neither is the case. As the table shows there are no more cases of CJD in Britain, which has by far the highest incidence of BSE, than in other European countries where there is none. (5) The Netherlands, which has no BSE, has more deaths from CJD than we do; and Finland, with few if any cattle, has nearly twice as much CJD.
| Finland | France | Germany | Italy | Netherlands | Switzerland | UK | |
| CJD cases per million people, 1993 | 0.9 | 0.50 | 0.47 | 0.54 | 0.68 | 0.9 | 0.56 |
| Total cases of BSE up to 1993 | 5 | 1 | 0 | 0 | 12 | 121,685 |
And CJD is not increasing. In 1984, the year before the first case of BSE in Britain, there were forty-two deaths in England and Wales; in 1993 there were only thirty-four. (6) Much is made of four cases of CJD in farmers who have had BSE in their herds, but this is a red herring: there have been six deaths in clerics. (7) And there are cases of CJD in lifelong vegetarians we aren't told about. The modern abattoir uses chainsaws to cut up animal carcases. These are cooled with jets of water which splash beef 'sawdust' all over the place. Yet there have been no deaths from CJD in abattoir workers, or in vets and others who have a much more intimate relationship with BSE infected tissue.
About fifteen percent of all cases of CJD are known to be hereditary, passed from one generation to the next. (8) All the rest of the cases appear to be caused by doctors. From all over world come reports of CJD in people, including children, given human growth hormone (9) and other human tissue – sex hormones, corneal transplants, dura mater grafts. (10) There is no suggestion that a single case of CJD has been acquired from either eating or working with a BSE infected animal. (11)
Further evidence that BSE could not be passed to humans was demonstrated in December 1995 using mice with implanted human tissue. While BSE did transfer to the mice without the implants, it did not to those with it.
Sheep have suffered a similar disease, scrapie, for over 200 years, with no evidence that it transferred to humans. Nevertheless, to minimise any risk, in 1989 the British government banned the use of cows' brains or spinal cord, the only parts of the animal which contain the BSE agent, from use in any food product.
In 1993 the World Health Organisation concluded that the BSE epidemic in Britain was over and that UK policies were sufficient to minimize the risk of exposure to BSE of all species, including humans. (12) The BSE scare should have been over.
Variant CJD
But then along came 'variant CJD' (vCJD). This differed from the original CJD and was more like the form that occurred in cattle. It was decided that this could be blamed on eating contaminated beef. But, still there was no proof of this. The fact was still that nobody knew where vCJD originated or what caused it. That it came from infected beef was still just a guess.
All living organisms mutate or evolve. Why should CJD be any different? It could be that vCJD is merely a mutation of 'normal' CJD.
Did the 'experts' cause BSE?
Somerset organic dairy farmer, Mark Purdey, had always been sceptical of the hypothesis that cattle eating infected meat was the cause of BSE or that eating beef caused CJD.
Purdey's research indicates that the mad cow disease epidemic in England occurred in areas where farmers were forced to treat their cattle with organophosphate pesticides in a warble fly eradication program. (13) The warble fly makes holes in the cows' backs. While that is not dangerous in itself, it reduces the value of skins sold to leather manufacturers. But these holes are also weak spots as far as infection is concerned. While sheep are completely immersed (dipped) in organophosphate pesticide, the pesticide mandated by government for warble fly treatment, it is poured onto the backs of cattle — along their spines. Any warble fly holes will facilitate the pesticide's passage to the spinal cord and organophosphate pesticides are very toxic to the nervous system. By a complex process, these compounds seem to cause certain proteins to fold in pathological ways. These are the 'prions' that are found in the brains of cattle with BSE and humans with CJD. According to Purdey, certain minerals in the environment are also involved: particularly high levels of manganese coupled with low levels of copper. Purdey's travels around the world have disclosed that both clusters of human CJD cases and BSE are found in areas where the soil has such mineral imbalances – areas where there are cement factories and where high levels of organophosphate insecticides have been used.
Purdey has incurred the wrath of the Ministry of Agriculture for refusing to dip his sheep or use organophosphates on his cattle. And, although farms around him have had cases of BSE, he has not had one.
Needless to say, the Ministry refuses even to consider Purdey's work.
To sum up CJD and BSE: These diseases are only passed genetically within families or by feeding or transplanting infected material within the same species: BSE passes from cow to cow; CJD from human to human. There is no evidence that the one causes the other.
The time to give up eating something is when there is the greatest risk. If there ever was any risk in eating beef, that time was well over a decade ago. And as there is actually no evidence that anyone was at risk then, it makes no sense to give up eating beef now.
Foot and Mouth Disease
Foot and mouth disease is a highly infectious viral infection which affects all cloven-hoofed animals: cattle, pigs, sheep, deer, and so on. There are no health implications for humans. As a disease foot and mouth disease is no more dangerous to these animals than flu is to us. Animals which contract foot and mouth disease form blisters on their feet and in their mouths. These are uncomfortable. They make walking difficult and it makes the animals froth at the mouth. While it is not pleasant, it is rarely fatal; most animals recover within a couple of weeks.
In many areas of the world, foot and mouth disease is endemic.
It is in southeast Asia, for example. There are some eighty million pigs in Hong Kong. Because of the prevalence of foot and mouth disease all pigs there are vaccinated. The vaccination doesn't protect them all; in any one year a couple of thousand still contract the disease and one or two die — out of 80,000,000, that is not many. Nobody worries about eating pork in Hong Kong because there is no risk whatsoever, in so doing.
Britain has been free of foot and mouth for decades. In 2001 it reappeared. The government set about its eradication by killing all sheep (mainly) over a radius of two miles from each case. Vaccination was not seriously considered.
By the end of the first month, foot and mouth was finally admitted to be out of control. At that time it was estimated that the cost in terms of killed livestock, and ruined businesses, particularly in the tourist industry, was already more than a billion pounds. And this was set to rise even higher as the experts predicted that the disease wouldn't peak for another three months and involve ten times as many cases.
Vaccination
Vaccination would have saved billions of pounds; it would have saved millions of animals' lives; it would have prevented bankruptcies in the farming community; it would have saved farmers from committing suicide; it would have saved the tourist industry; it would have saved people's livelihoods, it would have saved our reputation abroad. It wasn't done because a vaccinated animal could still be a carrier of the foot and mouth virus, the excuse given: it wasn't done because a vaccinated animal could not be exported and "our export markets would have been harmed" according to the National Farmer's Union.
But this is a ridiculous argument that would have been seen through straight away if those in government had had any knowledge of economics and the countryside.
Britain's meat and live animal exports were reputedly worth £507 million a year. It was solely to protect this that vaccination wasn't seriously considered. But this, surely, is bordering on criminal lunacy. £507 million may seem a lot but tourist and rural industries alone were losing that much every two weeks. And for what?
Firstly, it didn't save our export industry — we couldn't export animals or meat. After the BSE scares, this foot and mouth fiasco has further damaged foreign confidence in our meat. But even if we manage to return to exporting £507 million of meat and livestock, it will take several years merely to recoup the billions this crisis cost.
Secondly, Britain exports 195,000 tons of pork to the EU — but we import 240,000 tons from them.. Britain also exports 102,000 tons of lamb to the EU — but imports 125,000 tons from them. So why do we need to export pork and lamb!
The truth is that we do not need to export this meat and so the argument that vaccination would stop our exports was totally irrelevant.
On 28 March 2001 the EU gave Britain permission to vaccinate a limited number of animals. Why did we need to ask them? If I want a flu vaccination, I don't ask the EU first; I don't even ask my local council. And they don't tell me.
To its credit the EU moved swiftly in giving this permission. But, judging from BBC news programmes, the British government did not. What stopped them. At the rate they were moving and with the measures they were taking, the halt to the spread of foot and mouth was beginning to look as if it would only come with the slaughter of the last cloven-hoofed animal in Britain.
Conclusion
Clearly, the 'experts' need to be more open-minded and consider that they may not always be right. They need to listen to others outside their very narrow field. Mark Purdey committed the ultimate sin. He tried to tell them that they might be wrong. No 'expert' would listen to someone who was 'only' a farmer. Yet if Mark Purdey's hypothesis had been considered earlier, who knows how much grief it might have saved. It has still to be proven beyond doubt, but it is a much more likely hypothesis than that which the 'experts' have managed to come up with. Purdey went out and tried to discover the cause of BSE and CJD; the 'experts' merely sat around a table and discussed it.
It's the same story with the foot and mouth epidemic. Firstly, government machinery ground so slowly that the epidemic had really taken off before anyone thought to do something about it. But, after that, the wrong strategy was taken. Nobody, it seems, bothered to work out the consequences of a mass cull. It might have seemed like a good idea at the start of the outbreak but, surely, it need not have taken a month to come to the conclusion that this approach wasn't working.
What we need advising government is not 'experts' with tunnel vision, but common sense.
For the future
We can only speculate on what brought foot and mouth to Britain. It may be contaminated illicit meat imports from the Far East which got into pig swill as has been suggested, or it might have been something else entirely. But that one event sparked off the epidemic and it is the EU that must carry a large proportion of blame for the initial spread of the disease: it was their rules which mandated it.
Every county used to have several small abattoirs which catered to the local farming community. Animals were brought to them a short distance with the minimum of distress to the animal. But that was not good enough for EU bureaucrats. They insisted on a vet being present to monitor each animal's slaughter. And these vets had to be paid. This put up prices and made it uneconomic for the small abbatoirs. They went out of business leaving just a few large abbatoirs.
The lack of local abbatoirs meant that animals now had to be transported over long distances from the farms for slaughter. Not only did this mean considerably more disturbance and stress for those animals, it also meant that a disease in one part of the country could be spread over large distances by the transporters. And so it proved as it was this transportation that spread foot and mouth.
We need now to forget about UE rules, formulated by ignorant bureaucrats, and get back to traditional methods. That appears to be the only way to bring some sanity back to farming.
References:
1.
Professor Richard Lacey.
The Time, The Place
. ITV, 12 December 1995.
2.
Mocsny N. Precautions prevent spread of Creutzfeldt-Jakob disease.
J Neurosci Nurs
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23(2): 116-9
3.
Kretzschmar HA, Neumann M, Stavrou D. Codon 178 mutation of the human prion
protein
gene in a German family (Backer family): sequencing data from 72-year-old
celloidin-embedded brain tissue.
Acta Neuropathol Berl
. 1995; 89(1): 96-8
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Marsh RF. Bovine spongiform encephalopathy: a new disease of cattle?
Arch Virol Suppl.
1993; 7: 255-9
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Alperovitch A, Brown P, Weber T, Pocchiari M, Hofman A, Will R. Incidence of
Creutzfeldt-Jakob disease in Europe in 1993.
Lancet
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Registrar General's Mortality (Cause) Statistics, 1984, 1993; International
Classification of
Diseases 046.1. HMSO, London.
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Brown P, Cathala F, Raubertus RF,
et al
. The epidemiology of Creutzfeldt-Jakob disease:
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literature.
Neurology
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Zilber N, Kahana E, Abraham M. The Libyan Creutzfeldt-Jakob disease focus in
Israel: an
epidemiologic evaluation.
Neurology
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Billette de Villemeu T, Pradel A. Iatrogenic Creutzfeldt-Jakob disease.
Lessons from cases
secondary to extracted growth hormone in France.
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1994; 1(5): 333-7
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Brown P, Cervenakova L, Goldfarb LG, McCombie WR, Rubenstein R, Will RG,
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Neurology
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Ridley RM, Baker HF. Genetics of human prion disease.
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Purdey M..
J Nutr Med
1994; 4: 43-82
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