WHEN the former agriculture minster John Gummer fed his six-year-old daughter a hamburger during the BSE crisis, it was to show that there was no risk of bovine spongiform encephalitis being passed to human beings. We now know that the same prions — or malformed proteins in the meat — that cause BSE can cause a human version known as new variant CJD, but nvCJD seems to be extremely rare.

Could the Gummer hamburger, however, have posed the threat of a far more common disorder? According to a highly controversial book published next month, prions could also be the cause of Alzheimer’s disease.

The book, already published in Canada and criticised by both the meat-packing industry and the Alzheimer’s establishment, is entitled Dying for a Hamburger: how modern meat-packing led to an epidemic of Alzheimer’s disease. Co-written by Dr Murray Waldman, a Canadian coroner and researcher at the University of Toronto, it raises a number of worrying questions about an incurable condition that currently threatens 20 per cent of people over 80.

Waldman begins by asking: “Is Alzheimer’s a new disease?” Although its cause is unknown, most accounts tend to assume that cognitive decline has always been associated with growing old. However, Waldman’s review of pre-20th-century literature shows no evidence for our assumption that old age goes with mental decline. In fact, the medical definition of “senile” did not include “dementia” until 1962.

Most remarkably, the number of articles on Alzheimer’s disease in medical journals increased by 5,000 times between 1966 and 2000, compared with six times and four times for prostate cancer and heart disease. “It is hard to avoid the conclusion that Alzheimer’s is a new disease,” Waldman writes.

The villain, he claims, is some sort of prion, an abnormal protein found in brain tissue which clumps together with other proteins and is responsible for certain rare neurological disorders known as “prion diseases”.

To begin with there is guilt by association. The similarities between Alzheimer’s and prion diseases — BSE/nvCJD are not the only ones — include taking a long time to emerge, driving their victims mad and being associated with plaques and tangles in the brain. What’s more, cases of nvCJD can be misdiagnosed as Alzheimer’s and vice versa.

Crucially, there is the fact that Alzheimer’s emerged in the wake of the industrialised farming and meat-packaging production-line techniques that allowed the BSE prions to get into the food chain. Where these techniques have been introduced, first in Europe and America and more recently in the countries of the Pacific Rim, processed meat consumption has soared along with rates of Alzheimer’s. Waldman points out that levels of Alzheimer’s in largely vegetarian India are still very low.

He makes a fascinating case based on circumstantial evidence, but it lacks a smoking gun. The clincher would be if it were possible to inject tissue from the brains of Alzheimer’s victims into animals and recreate the disease in them, as can be done with nvCJD. Research of this kind has not been undertaken in the UK but experts here are adamant that it cannot be done, and that Alzheimer’s is not a prion disease.

“Both diseases involve proteins in the brain that somehow change shape and cause damage,” says Dr Susanne Sorensen, head of research for the Alzheimer’s Society. “But they are different proteins and the diseases have a different biochemistry and a different pathology.” Her explanation for the link with raised meat consumption is that this is a marker for the Western high-fat diet that is also blamed for heart disease. “Many of the risk factors for heart disease also apply to Alzheimer’s,” she says.

Whether or not Waldman is correct, he is not alone in suggesting that Alzheimer’s could be an infectious disorder. Ruth Itzhaki of the University of Manchester Institute of Science and Technology has shown a link with the hepatitis C virus. However, she and others complain of the hostility of the Alzheimer’s establishment to any challenge to the orthodox view, which is that the damage to the brain is caused by tangles of proteins known as “plaque”.

Earlier this year, for instance, The Wall Street Journal reported on the difficulties that a leading researcher at Harvard Medical School had in publishing work suggesting that plaque was actually protective.