Skip to comments.Link Between Mad Cow Disease and Human Deaths Questioned (BSE May Not Cause nvCJD)
Posted on 12/25/2003 1:28:53 PM PST by Pubbie
Mad cow disease strikes fear into the hearts of meat lovers everywhere, and with good reason. Although slightly more than 100 deaths have been attributed to eating contaminated beef, some researchers speculate that millions of people may one day fall victim to the fatal human form of the disease as a result of eating a single tainted burger or steak.
But provocative new research questions the link between infection in cattle and that in humans. Writing in the Oct. 13 issue of the British Medical Journal, Scottish epidemiologist George Venters, MD, of NHS Lanarkshire, argues that there is no clear evidence to prove that mad cow disease can be transmitted to humans by ingesting contaminated meat products. He adds that the case for such transmission is weak.
"This will undoubtedly be controversial within the scientific community, but that is part of the point," Venters tells WebMD. "I want to prompt more appropriate explanations about what is going on here than the facile one of infection. The infectivity hypothesis is, in fact, becoming a bit threadbare."
Mad cow disease, known medically as bovine spongiform encephalopathy (BSE), was first identified among British cattle in 1986 and has since spread throughout Europe. Since the mid 1990s, scientists have become increasingly convinced that a recently identified, rapidly degenerative, fatal brain disease in humans called new variant Creutzfeldt-Jakob disease (CJD) is caused by eating the meat of infected cattle.
Venters says there may be nothing new about new variant CJD. He suggests the cases classified as such may actually have been classical CJD, which is not a food-borne illness at all.
"If you have a food-borne infection, you expect the number of cases to rise at the same rate as the population was exposed to the infection," Venters says. "That has not happened here. People try to explain this by saying there may be a long incubation period, but the fact is that you have had cases occurring for seven or eight years now and the numbers have not been increasing."
Venters calls new variant CJD "the epidemic that never was," because its numbers have not increased dramatically in the years since it was identified. Using established research methods, Venters says he could find no direct evidence that the infectious proteins known as prions, which cause BSE in cattle, are infectious to humans.
"It is unlikely that human beings who eat prions from other species are likely to get infected, because our own defenses are well enough organized to digest or to destroy these prions," he says.
But prion researcher Robert B. Petersen, PhD, disagrees and says while some of Venters' assumptions may seem valid on paper, they just don't reflect what is going on. Petersen says studies have shown that the molecular signatures of BSE and new variant CJD are virtually identical. And animal studies have confirmed the pathological similarities of the two diseases. Petersen is an associate professor of pathology at Cleveland's Case Western Reserve University and is chief scientific officer for a company working to develop a diagnostic test for BSE.
Petersen tells WebMD that by looking at all the features of the disease, it's clear that there are different types of CJD. The new variant CJD doesn't appear to be like anything that occurred before doctors started to study BSE.
People may argue that by now, doctors should be seeing more people sick with variant CJD, Petersen says. But in order to make such an assumption, scientists have to know a lot more about the disease than they do today, such as how long it takes to show signs of the disease after becoming exposed to it. That period of time could be anywhere from 10 to 60 years, Petersen says. "We just don't know at this point."
Similarly, there is no way to know whether an epidemic of new variant CJD will occur in years to come among people who may have already been infected, he says.
Thanks for posting this article.
I think I'll go make more room in the freezer.
Upper limit is 60 years? Would this put the average range around 30-40 years then? I think I'll keep snarfing Big Macs...
Then why do cannibals who eat brains develop kuru?
Yes but we all have the normal folded protein. Is it possible that the vCJD prions assumed its characteristic conformation independent of interaction with BSE prions?
Might you provide references on the pathologic research that shows what you describe?
Regular CJD strikes approximately one person per million in any world-wide population. It often effects the elderly and disregards socio-economic levels, race, nationality etc. and has nothing to do with diet. vCJD was a strain of CJD that showed some differences, it attacked younger people for instance, and was first diagnosed in Europe in the late '80's, when scientific evidence began to suggest a possible link between vCJD and BSE in cattle. This became a political issue in Europe that was quickly blown into a major health scare, predicting 10,000 deaths from vCJD by 2000 with another 1000-2000 new cases each year after that. But in fact, none of these dire predictions ever materialized.
To date, 137 deaths worldwide have been attibuted to vCJD since the late 1980's. Six other known cases are in people who are still living. There has never been a confirmed vCJD case in the US except for the woman who contracted the disease in Britain but came back to FL to be with her family when she died.
"Virtually identical" means "different."
The disease in experimental animals is the same for BSE and vCJD.
No, it means that both are quite different than CJD.
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