Minerals link BSE to OPs

14 January 2000

‘Minerals link BSE to OPs’

By Isabel Davies

CLAIMS that BSE was triggered by a mineral imbalance caused by organophosphate pesticides may be investigated by the government.

This theory is at variance with the widely-held view that contaminated meat-and-bonemeal feed caused the cattle epidemic.

Farmer Mark Purdey, from near Taunton in Somerset, has spent years unsuccessfully trying to interest MAFF in his theory.

But now the government is believed to be considering his view that BSE is triggered when high manganese co-exists with a copper deficiency.

The revelation comes as a Swiss team claims it has discovered a substance which could reverse the effects of BSE in humans.

Mr Purdeys theory is based on his research in Colorado, Slovakia and Iceland, where analysis of soil and vegetation showed mineral imbalances.

Metal manganese levels were two-and-a-half times higher than expected, while copper levels were unusually low, he said.

Mr Purdey claims this indicates BSE was caused by the mineral imbalance, and that experiments carried out at Cambridge University seem to support this.

Researchers found that if a prion protein is exposed to high levels of manganese, it changes shape.

Many researchers believe “rogue prions” which fold the wrong way are responsible for causing BSE and related diseases.

Mr Purdey claims the OP Phosmet made cattle more susceptible to BSE because it starved prion protein in the brain of its normal copper requirement.

If an animal suffering a copper deficiency created by Phosmet consumed large quantities of manganese, a spongiform disease could develop, he argues.

If manganese or nickel were found on the prion proteins, this would almost certainly prove his theory, Mr Purdey claims.

Meanwhile, Swiss researchers have identified a process which reverses the characteristics of CJD and related spongiform diseases such as BSE and scrapie.

This prevents the formation of a destructive matter called “beta sheet” which result from rogue prions.

The new process centres on a peptide – or protein component – that blocks the formation of the beta sheet.

In experiments peptide reversed the structure and properties of rogue prions brains to a form similar to the original “safe” prion.

Studies on mice showed peptides delayed infectivity by up to 95% and greatly delayed the onset of symptoms.

But the says the teams, from the Serono Pharmaceutical Research Institute, do not yet know if the treatment achieves the same results in people.

New variant CJD, which is linked to BSE, has claimed the lives of at least 48 people since it was first identified.

Research published this week in the British Medical Journal confirms that the rise is genuine and free of statistical error.

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