| Eating is a risky business. You may choke on
an olive, contract cancer from celery or
coronaries from chips. Eat too much and you are
threatened with obesity; too little and anorexia
looms. Driving home from the restaurant may prove
to be the most hazardous activity of all.
Suddenly, beef is back in the news. Few
scientists are surprised to learn that there is a
new strain of CJD (Creudzfeldt-Jakob Disease, the
human equivalent of mad cow disease). There
isn’t any firm evidence to confirm that this
new form arose from cattle, though it’s a
reasonable guess it might. The most famous
victim of BSE was Daisy, a black and white
Friesian suckler cow aged six years. She is the
unfortunate beast who falls about so dramatically
in that early video of mad cow disease which
regularly re-plays on TV. You can see her trying
to rub her head with a hoof; you can see she can
hardly walk. BSE is a dramatic disease. It is
highly photogenic. It damages the brain. The
situation is a classical case, bound to attract
maximum attention. The government are the target
for attack on all sides. They should have known
better. They should have done more. We should
never have believed them ... yet how often do we
stop to reflect on the impossible situation a
government faces when there is a new threat like
this?
The way of politics is to set down principles
in black and white: “Is the Minister aware?
Yes or no?” - we hear it every day on the
Today programme, watch it each night in
parliamentary reports. Admitting that an opinion
may have been wrong, or having the grace to
change your mind, can be a resigning matter in
parliament. Scientific issues cannot be measured
in terms like those. In BSE the unknowns are
intriguing, and the science remains vague. You
often hear of the ‘virus’ of mad cow
disease. I have news for you: there isn’t
one. The cause of BSE is still a mystery. Viruses
contain DNA or RNA, and the agent of BSE contains
neither. It survives boiling. It is not even
attacked by disinfectants, and you need to heat
it in highly corrosive solutions to inactivate
it.
In sections of tissue under the microscope you
can see fine threads called prions. We do not
know what they are. Indeed, although it’s
comforting to assume that the prion causes the
illness, we don’t even know that. Maybe
prions form as a result of the disease. They
could be a symptom, and not the cause. There are
many such diseases. The first to be written about
was scrapie (so called because sheep scrape
against walls and fences as they become ill). It
turns up as far back as 1759, accurately
described by a German vet named Leopold. Nothing
new there, then. Kuru is a similar human disease
first described in 1957 among the cannibals
living in the eastern highlands of Papua/New
Guinea. It has died out with cannibalism.
Then came Daisy in 1987. What was the
government’s response? First, they did
nothing. They even passed word round that BSE was
not to be referred to in the same context as
scrapie, in case people got the wrong idea - and
then they made a crucial error. They should have
offered a premium price for farmers who found BSE
in their herds. They didn’t. In consequence,
every farmer with a suspect cow was losing money
when the slaughterman arrived. Cows in the early
stages were quickly sold, which soon spread BSE
right across the country.
In most infections, animals manifest the
disease throughout the body. Evidence suggested
that BSE might be confined to the central nervous
system, so the government made slaughterhouses
remove the main nerves from infected carcases,
and stain them so that could not be used in food.
This is the era of market forces, and dyes
cost money. So does the time to do the work, and
experienced slaughterhouse staff. In the real
world, cheap labour is often used, so there is
nobody around to ensure the task is done
properly. The removal of offal is often hastily
done, to save time. And I am not aware of any
mechanism for ensuring that none of the condemned
by-products ended up in cheap sausages and pies.
Indeed, I cannot even imagine how such a system
could be made to work in an era hungry for money.
One of the reasons why most scientists did not
believe there was a link between BSE and people
is because of the comparison with scrapie. There
is about one case of CJD in a million people
every year, give or take a few. The important
point is that this is the rate in countries (like
ours) where scrapie has been found for centuries,
and is exactly the same in others (like
Australia) where the disease is absent. That
alone tends to make one conclude that at least
one form of spongiform encephalopathy is not
transmitted to humans.
What can government learn from all this? They
could start by recounting the reality. Several
major official reports have advised against
saturated fat - so sales of fatty foods go higher
by the minute. We have been told to cut back on
salt, since when sales of crisps and other salty
products have mushroomed in schools and are
rarely missing from the lunch-box. There are
several known risks from hamburgers, including
the problems posed by the fat and new strains of
food poisoning which are difficult to treat.
Those risks are far greater than those from BSE.
The public have always ignored authoritarian
advice from official sources; British people do
not like to be bossed.
If there is any single lesson, it is that
people often do the opposite of what they have
been told. The greatest problem for farmers is
that the government advised everyone beef was
bound to be safe - had they warned against it, I
dare say sales would have doubled in a month.
People like facts. They suspect official
propaganda. Just as well-known as the sight of
poor Daisy staggering in the farm-yard is the
propaganda clip of John Selwyn Gummer, stuffing a
hamburger into his daughter’s mouth. How odd
that one knows the name of the cow, and not that
of the little girl. I pray it stays that way.
Brian J Ford has written several books
on food, and presented Food for Thought
on Channel Four TV.
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