It hardly mattered what was said about beef and Bovine Spongiform Encephalopathy (BSE) at Westminster yesterday. The mere linkage in words between BSE and Creutzfeldt Jacob Disease (CJD) will be enough to deter another large tranche of consumers from eating beef, despite the fact that there is still no clear scientific evidence to support that verbal linkage. And any such deterrence must have a serious effect on the beef industry, an industry upon which the economy of Ireland, never mind Britain, is seriously dependent. Most worried consumers will not take the time or trouble to make distinctions between British beef, where levels of BSE have been quite high in the herd, and Irish beef where levels have been low.
It was scarcely to be expected that yesterday's exchanges in the House of Commons were going to clarify the situation for farmers, butchers or consumers. The ambivalent muddle which has been characteristic of the British government's handling of BSE all along, was all too evident again yesterday. Yes, British beef is safe to eat, it was said. But not, apparently, safe enough to prevent further regulations: being introduced to cover the safer de boning of slaughtered animals and the exclusion of bonemeal and animal protein from the animals diets. Yet there is no evidence to prove that BSE can be transmitted from animals to produce CJD in humans.
Most students of logic and science know that it is impossible to prove a negative. It will never be possible to demonstrate conclusively that BSE has never induced a case of CJD. Indeed, CJD itself is not yet fully understood in every detail. It is thought that BSE was introduced to herds through the feeding to animals of bonemeal or other products contaminated with an infective agent from sheep suffering from scrapie (a disease not unlike BSE or CJD). Yet before BSE came along there was never a suggestion that humans developed CJD as a result of eating sheepmeat.
The arguments are almost circular and repeatedly inconclusive. None of them has been resolved by yesterday's British government statements. Even the revelation that a sub group of 10 new cases of a CJD like disease in humans has been identified, adds little clarity to the situation overall. One of the distinguishing characteristics of these new cases is that they have occurred in a group with a much younger average age (early 20s) than classic cases where the average age is the early 60s. The suggestion that they might have a dietary cause is plausible, and it was pointed out that they developed before the British ban on the feeding of animal offal was effected in 1989. Yet the brain pathology is significantly different from that found in BSE.
Perhaps the most encouraging development in yesterday's statements was the announcement by the British Secretary for Health, Mr Stephen Dorrell, that he was investing £4.5 million in further research into the dilemma. This might give rise to clearer insights into the various human and animal diseases involved in the arguments. Meanwhile, the very least that this State needs to do is to emphasise the healthy differences between the Irish and British products. Some reassurance may be taken from the data which show that, even if there were to be transmission from animals to humans, the risks are very small indeed. But it bears repeating that there is no scientific evidence to prove that such transmission can occur.