Even by 1990, when the epidemic curve was on the upswing, questions were raised in many quarters in the UK, "...does BSE pose a risk to human health?" British government officials at the time said don't worry, there is nothing to worry about. This of course only led the public to become more skeptical. Even then, in 1990, the editors of the British journal Nature reacted, saying: "...Never say there is no danger {risk}. Instead, say that there is always a danger {risk), and that the problem is to calculate what it is. Never say that the risk is negligible unless you are sure that your listeners share your own philosophy of life..." I think this advice has come back to haunt British officials again, six years later.

On March 21, 1996 10 cases of CJD in people not otherwise considered at high risk were announced.
These individuals were much younger than the usual cases of CJD that occur sporadically everywhere in the world at an incidence of about one per million population per year. This sporadic incidence of CJD is the same even in countries, like Australia, where there is no scrapie. Also, there have been statements in the press, but no details, that the pathologic changes in the brains of these 10 patients are different from those in usual CJD cases. In any case, it is the age-distribution of these 10 cases (average age 27 vs. 63 for sporadic CJD cases) that led the British expert committee to make its startling announcement.

In order for the hypothesis that vCJD is caused by eating beef products contaminated with defective prions a number of conditions would need to be true.

1. Compatibility between bovine prions and human prions. That is that the bovine abnormal prion can distort a normal human prion.
2. That the frequency of human consumption of abnormal prions has increased.
3. That prions can migrate from the stomach to the brain

This can be taken as proven. Experiments with mice having been with genetically modified with human prion producing genes have shown that prions can cross the species barrier.

When BSE was widespread in the UK, the opportunity to eat infected material was very high before procedures were put in place to prevent the source of infected material entering the food chain.

The issue of frequency is important.
Genes produce prions. Bovine prions are sufficiently similar to human prions as to be able to say that the appropriate bovine genes are similar to human ones. Human genes can spontaneously produce CJD so it would be reasonable to expect bovine genes to behave likewise. That being the case, spontaneous outbreaks of encephalopathies should be expected to occur in cattle. A well-known condition is known as the shakes, symptoms similar to BSE.
Occasional outbreaks, within normal expectancy, would indicate no more of a threat through frequency than has existed since humans began eating bovine products.

So the remaining issue is the effectiveness of the gut barrier. If the barrier were 100% effective, all the other issues disappear - prions would be unable to migrate to the brain no matter how common they were in food. Nothing is 100% effective, so is the gut barrier sufficiently effective. Cattle, being herbivores, are afforded no such protection so when their food had an increased occurrence of abnormal prioms the rate of TSE infection also rose.