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New Theory on How Mad Cow Disease Started

Controversial Theory: Roots in Human Disease

From the WebMD Archives

Sept. 1, 2005 -- A new theory on the origins of mad cow disease is sparking debate in The Lancet.

The theory traces the seeds of mad cow disease back to humans. But it doesn't have solid evidence behind it. No one knows how bovine spongiform encephalopathy (BSE, or "mad cow" disease) got started.

The husband-and-wife scientists who propose the theory admit that. They don't claim to have solved the mystery.

They are Alan Colchester, FRCP, of Kent Institute of Medicine and Health Sciences at the University of Kent in Canterbury, England, and Nancy Colchester, MBChB, of the University of Edinburgh College of Medicine and Veterinary Medicine in Scotland.

Human Origins?

First, the Colchesters shoot down the notion that the disease may have started with scrapie, a usually fatal nervous system disease in sheep. There's "no convincing evidence" of that theory, write the Colchesters.

Next, they outline another possibility: Maybe mad cow started in the Indian subcontinent when ground-up bones of sick people wound up in animal feed that was shipped to the U.K., where the disease eventually became BSE.

The human illness must have been a "prion" disease, write the Colchesters. Prion is a protein that has been tied to mad cow disease. In humans, mad cow disease is called variant Creutzfeld-Jakob disease.

Bone Beginnings

How do the Colchesters explain how human bone might have gotten into British animal feed?

They write that Indian and Pakistani peasants sometimes gather large bones from land and rivers to sell, and that "Hindus believe that it is essential for their remains after death to be disposed of in a river, preferably the Ganges."

"The ideal is for the body to be burned, but most people cannot afford enough wood for full cremation," the Colchesters continue.

During the 1960s and 1970s, the U.K. got a lot of raw material for fertilizers from Bangladesh, Pakistan, and India, write the Colchesters. Some of that raw material could have included human bones and may have been mixed into animal feed, despite rules to the contrary, they theorize.

In other words, the Colchesters suggest that humans already had variant Creutzfeld-Jakob disease, passed it on to cows through ground-up bones in animal feed, and then the cows gave it back to people.

Jumping to Conclusions?

An editorial in The Lancet punches holes in the Colchesters' theory. The editorial comes from Susarla Shankar, MD, and colleagues from the National Institute of Mental Health and Neurosciences in Bangalore, India.

"So far, not a single case of BSE or scrapie has been reported from India, except for one case of scrapie from the Himalayan foothills in a sheep, which was probably imported," they write.

The editorialists also dispute the bodies-in-the-river theory.

"By the Colchester's extrapolation, 150 deaths in India are related to Creutzfeld-Jakob disease. In most of the hospital-related deaths, the bodies are not taken to Varanasi, the holy city on the banks of the Ganges in North India, but [are] cremated or buried in community burial grounds," they write.

"Even in Varanasi, most Hindus do not put half-burnt bodies into the river. The Colchesters have drawn heavily from pictures on the Internet and other sources," the editorialists continue.

There's also no proof that cattle could get the disease from ground-up human bones, they write. The Colchesters agree with that point, and they call for tests to see if it's possible.

Proceed With Caution

"Scientists must proceed cautiously when hypothesizing about a disease that has such wide geographic, cultural, and religious implications," write Shankar and colleagues.

"We agree that the idea proposed by the Colchesters needs to be probed further. Facts to support or refute their hypothesis now need to be gathered with urgency and great care," they conclude.

WebMD Health News

Sources

SOURCES: Colchester, A. The Lancet, Sept. 3, 2005; vol 366: pp 856-861. Shankar, S. The Lancet, Sept. 3, 2005; vol 366; pp 790-791. News release, The Lancet.
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