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The metal detector

February 4, 2002 The Times (London) by Anjana Ahuja
Anjana Ahuja talks to the man who says there is no link between BSE in cattle and vCJD in people

Dr David Brown is not your usual scientific maverick. The biochemist has held positions at respectable universities -including Cambridge -and seeks little publicity for his work.

But his ideas are controversial. Brown does not buy into the scientific wisdom that the human form of "mad cow" disease (variant Creutzfeldt-Jakob disease, or vCJD) is caused by people eating meat infected with bovine spongiform encephalopathy (BSE). That sets him against 95 per cent of the research community and against the Government, whose inquiry more than a year ago concluded that the link between vCJD and BSE was a pretty much open-and-shut case. Brown, who runs the Centre for Prion Research at Bath University, suspects that the metal manganese could be implicated. He knows that his could be a voice in the wilderness, but he is willing to risk being marginalised. "I'm not saying that manganese is the answer, but more open-minded scientists are saying that it has to be examined," he says.

The chances are that his suspicions will turn out to be unfounded, but he has won the backing of the Prince of Wales and a six-figure sum from the Government to explore them. He may also be encouraged by the fact that study in this area has already been revolutionised by a scientific loner.

In 1982, Stanley Prusiner, a biochemist at the University of California, encountered derision when he suggested that a rogue protein called a prion could be an infectious agent, rather like a bacterium or a virus. Fifteen years later he won the Nobel Prize for Physiology or Medicine -and today prions have, as it were, been welcomed into the pantheon of biological killers.

Prions lie at the heart of diseases such as vCJD and BSE -they are misfolded proteins in the brain that act as a dangerous template for nearby proteins, leading to a breakdown in the amazing biological origami that keeps brain matter healthy. The result is that the substance of the brain develops holes (this is why BSE and CJD are known as spongiform encephalopathies). In Britain, 104 people have died in this devastating way. A further nine are living with the disease.

BSE experts insist that there is a wealth of compelling circumstantial evidence to suggest that BSE causes vCJD: mice infected with one or the other develop identical, lethal patterns of damage in brain tissue; small clusters of the devastating brain disease could be traced to infected meat from a single source.

That doesn't wash with Brown. "I don't believe that BSE causes vCJD," he responds, adding that government measures have not yet eradicated BSE, which must imply a flaw in the biological chain of reasoning that leads from infected cattle feed to dying people. "We need to consider new theories."

He says that circumstantial evidence, however strong, is not proof. In fact, the only way of proving the link would be impossible -deliberately infecting people with BSE to see whether they developed vCJD. The Department for the Environment, Food and Rural Affairs (Defra) has awarded Brown a grant worth almost Pounds 200,000. Scientists who toe the orthodox line, however, dismiss his arguments as "soft".

So how has Brown fingered manganese as a possible villain in the vCJD saga? Late last year he compared the brains of nine people who had died of sporadic CJD(another form of CJD which arises spontaneously and mysteriously in one in a million people) with the brains of people who had died from other causes. The brains of sCJD victims contained about ten times as much manganese as the normal brains. He published in the Journal of Neurochemistry; the eminent weekly publication, Nature, turned him down "for no justifiable reason", he says. The Defra money will help him to conduct a bigger study to find out if high manganese levels are also found in the brains of vCJD victims.

Brown's theory is that, in those who succumb to the disease, the brain is unable to handle manganese properly. The metal binds to brain tissue and somehow strips away its defence mechanisms. The tissue, unable to fend off oxidative stress, then dies. There is a ready supply of manganese in the environment -in the soil, in vegetables -and so, Brown says, it should not be ruled out.

He has many bones to pick with the orthodox argument, such as the fact that vCJD came many years after BSE. "The chronology is meaningless," he insists. The first case of BSE was spotted in the late 1980s and the first vCJD case was seen in 1995. Human beings have a very long incubation period, Brown says, so the disease could have arisen sporadically in humans and cattle at the same time. Another mystery is why a handful of vCJD victims were vegetarians.

Brown continues: "Scientists found a cluster where four out of five people ate meat from butchers with similar practices. Why wasn't it five out of five? The butcher connection can't be the full story. It could be coincidence. If the numbers were larger, say 45 out of 50, I'd be more inclined to say there is something going on."

Such arguments have not found favour in the research community at large. Dr Moira Bruce, from the neuropathogenesis unit at the Institute of Animal Health in Edinburgh, was among the first scientists to show that both BSE and vCJD caused identical brain damage in mice. She rejects Brown's caveats.

"These are rather soft arguments," she says. "Proving something is always tricky in biology, but 95 per cent of scientists who have looked at this issue believe the balance of evidence points to vCJD being caused by BSE in cattle.

"If you were dogmatic, you could say that human beings acquired vCJD and cattle acquired BSE from independent sources, but it isn't likely. There were so many BSE-infected cattle, it would have been the major source of infection for people." She adds that identical markers have also been found in cats and in two antelope-like species (kudu and nyala); all would have eaten feed containing matter from infected cattle.

But Brown remains suspicious that elevated levels of manganese in the environment somehow cause vCJD. It must be a subtle effect, he says, because of the low numbers of people involved.

Yet if there were regions with high manganese levels in the soil or water, wouldn't one expect dramatic geographical clusters?

"Not necessarily, because people move around so much these days," Brown says, suggesting that a two-week visit to Edinburgh might, for example, expose one to a vCJD-causing agent.

If Edinburgh harboured such sinister dangers, wouldn't longstanding residents of the Scottish capital be widely affected? Brown concedes that this may be so, but says that since he knows nothing about the distribution of manganese in the environment, it is impossible to say what the geographical spread would be. He also says that any effect is likely to be subtle and might operate in tandem with another factor.

He adds that in Iceland, scrapie (the sheep equivalent of BSE) tends to be concentrated in areas where the vegetation has an extremely high manganese content, up to 1,000 times the levels in unaffected areas. "In Slovakia there is an active ferromanganese industry and the incidence of sporadic CJD is five times what you'd expect," he says.

Bruce rebuffs Brown's statistics. She says that the Slovakian clusters are genetic rather than geographical, and that scrapie was introduced into Iceland by a flock of sheep.

"There may be environmental factors that make sheep more susceptible to an acquired infection, but there is no evidence that scrapie just comes out of nowhere," she insists.

Brown is an associate of Mark Purdey, the Somerset farmer who claims that BSE is connected with an organophosphate used to treat warble fly in cattle. The treatment contains high levels of manganese. Purdey came into contact with Brown when the latter, then at Cambridge University, showed that manganese could bind to a normal protein and, at excessive levels, could turn it into an abnormal one (prion).

Brown remains unconcerned at the way his theory has been dismissed: "Some people say my work is rubbish but they're not very common now. The people I am working with don't tell me I'm crazy."

anjana.ahuja@thetimes.co.uk


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