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Mad cows and Englishmen

Recent research demonstrating a link between BSE and new variant CJD does nothing of the sort, claims Julian Morris

'Nobel scientist says link between BSE and CJD' screamed headlines immediately before Christmas. The news came four days after Lord Phillips, chairman of the two-year inquiry into bovine spongiform encephalopathy (BSE), said that the current death toll from the new form of Creuzfeldt-Jakob disease (CJD) could be 'just the tip of an iceberg'. But in a new paper for the Institute for Economic Affairs, Janie Axelrad, a research biologist specialising in BSE-type diseases, demonstrates that the evidence of a link between BSE and new variant CJD (nvCJD) is extremely weak.

There are several different theories about what causes BSE in the first place. The first, most widely promulgated is that BSE resulted from cows consuming meat and bone meal (MBM) infected with prions, a damaged version of a type of protein, present in large numbers in the brains of afflicted cattle, thought by some to be capable of self-replication and hence transmission or infection. This theory gained popularity for various reasons, not least of which was the ickiness associated with feeding ruminants parts of their brothers and sisters. But the infective prion theory has always been contentious; and Axelrad points to some specific problems with this particular explanation of BSE. For example, many farmers have reported BSE in cattle that have not been fed with MBM. Even if some are lying, it is implausible that cattle born several years after the 1988 ban on use of MBM (as many BSE cases were) would still have been fed on stockpiled supplies. MBM has a maximum shelf life of only a few months, after which time the risk of death by infection is considerably greater than any putative risk of BSE. From this it seems that either MBM is not the transmission vehicle, or BSE is not caused by infective prions.

An alternative argument claimed that sheep infected with scrapie (a prion disorder which is significantly different from BSE in both symptoms and pathology) had been fed to cattle. But no link has ever been shown. Injecting scrapie-infected brain matter into cows' brains causes a scrapie-like disease rather than a BSE-like disease: to argue that a less direct route of infection might cause a BSE-like disease would require extremely circuitous reasoning.

Axelrad argues that a more plausible theory for the cause of BSE is that it is an auto-immune disease. In afflicted cattle, she says, the cow's immune system is attacking parts of its brain, probably because it mistakes these parts for foreign matter. The presence of prions is then explained as a consequence of the disease rather than its cause.

It seems that most existing theories about BSE are inadequate. Yet drastic steps have been taken on the basis of them. And the recent evidence supposedly indicating a positive relationship between BSE and nvCJD actually does nothing of the sort.

This research, by Stanley Prusiner, the scientist who won the Nobel Prize for his discovery of prions, involved injecting nvCJD- and BSE-infected brain material into the brains of mice genetically engineered to express cow prions, as a result of which the mice became afflicted with a BSE-like disease. This work was inspired by earlier research, by Professor John Collinge of Imperial College, London, in which mice genetically engineered to express human prions were injected with nvCJD- and BSE-infected brains. Collinge had found that when these mice were injected with nvCJD-infected material they became afflicted with an nvCJD-like disease, but when injected with BSE-infected material there was no prion disease. Combining the results of these two experiments, we can conclude that while nvCJD might cause BSE, BSE does not cause nvCJD.

There has been an increase in the incidence of CJD over the past 10 years, and the emergence of a new variety of CJD suggests the presence of some new causal agent. But the lack of any significant increase in nvCJD cases over time indicates that this agent is not BSE. If BSE were to blame we would expect the pattern of incidence of nvCJD to mirror that of BSE, rising exponentially from a small number to a very larger number before peaking.

Why then the panic? Was it a plot by fundamentalist Christians to send us cowering to church on Christmas Day to beg forgiveness for our sins against nature? Unlikely. Was it a plot by a crazed sect of anti-capitalists seeking to demonstrate the evil consequences of the profit motive? This also seems implausible. More likely, the respective scientists were taking advantage of the controversial (and I would argue misguided) remarks of Lord Phillips to garner media attention, in the hope that it would enable them more easily to obtain funding for the next round of their futile search for a link between BSE and CJD.

The obsessive focus on prion infectivity and attempts to 'prove' a causal relationship between BSE and nvCJD has had tragic effects. It has caused enormous damage to the British cattle industry, leading many farmers to ruin and probably inducing more than a few suicides. And it has stymied our understanding of the real cause of both BSE and nvCJD, preventing us from knowing which action might usefully be taken to prevent future cases of these horrific diseases.

Julian Morris is director of the environment unit at the Institute for Economic Affairs, and co-editor of Fearing Food (Butterworth-Heinemann, £15.99)

BSE: A Disaster Of Biblical Proportions Or A Disaster For British Science? by Janie Axelrad is available from http://www.iea.org.uk/env/bse.htm

Reproduced from LM issue 127, February 2000



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