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1) Organophosphates (OPs) have been used all over the world for decades - how could they have caused BSE?
OPs per se don't cause BSE,CJD or Scrapie. They are not like infectious agents that produce a specific disease when you come into contact with them.There is a vast group of chemicals out there coming into the OP category and there are many variables at work when animals or humans come into contact with them : dose and timing of dose; formulation - systemic or non-systemic, oil or water based; exposure route ie.breathed in, oral, skin contact, vapour contact to eye, as foetus, pour on ; additional ingredients and impurities are often present; neuropathic or non neuropathic; LD 50 (toxicity); variable biochemistry. The principle cause of BSE, in our opinion, was the way we used a copper chelating OP, Phosmet - at 4x the maximum dose, in an oil based systemic formulation, poured on the cow's spine, bi-annually (with a voluntary follow up dose after a fortnight). This was unique to the UK. during the 80s.There were many other OP exposures at the time that played a smaller role and you have to consider the cumulative affect of all of them. There are other factors involved, the most important of which was/is the greater availability of Manganese in the bovine diet. see the Introductory Hypothesis and other pages on this site.
2) Does MBM have any relevance in the Purdey Hypothesis ?
Yes it does, but its too simplistic to consider MBM as a whole - it needs to be broken down into its relevant constituent parts and these then studied. Manganese, pesticide residues, copper and antioxidants, PrPbse and PrPscrapie are some of the key items on such an agenda.
It also needs to be considered in the context of diet as a whole.
We would consider Mn to be the most important of these as it is known to have been increased in MBM (as well in other dietary forms) in the eighties and its still a common supplement throughout Europe.The contribution of the Mn contained in the grazed forage is probably small : cattle have grazed high Mn pasture throughout evolution without developing clinical BSE.
We would consider risk to be greatly increased when very young calves/ foeti are exposed to high Mn in MBM or other source, as they cannot regulate uptake levels as effectively as adults : see the discussion on high Mn in infant soy formula.http://www.insightmag.com/archive/200106252.shtml
Pesticide levels increased in MBM due to the cessation of the solvent extraction method of rendering down cattle carcasses.
PrPbse, when at a high level in the eighties, may have played a small role in amplifying the disease, but my opinion is that in the context of food products the toxicity is greatly reduced.
We consider PrPscrapie is irrelevant because cattle have been exposed to it since scrapie first appeared 250 years ago- by cross grazing pastures.
3) What about the more recent MBM theory -The spontaneous mutation theory.
This theory was first proposed by the Royal Society committee on TSEs and it was favoured by the BSE inquiry.There is little science to support it and much to negate it. It proposes that a single chance mutation (not identified) in the prion gene in the 70s caused a UK cow to develop BSE- its remains entering the food chain as MBM and spreading and causing the epidemic from 1985 on in the UK and then gradually further into Europe.
The problems with this theory are that experimental work with MBM containing high levels of PrPbse did not cause any disease in cattle.This confirms the epidemiological picture in which the same MBM/high dose PrPbse never caused BSE in many countries to which it was exported. This theory cannot account for the continued upward trend of BSE in Europe and the continued existence of BSE in UK cattle.
As BSE spreads it has been necessary for proponents of MBM to invoke the pathogenicity of ever lower doses of the agent ( presumably now homeopathic doses) The problem with this is how do you explain all the high dose Prpbse not causing the disease.
The sudden emergance and establishment of BSE over a short period of time 18 months with a wide distribution over the UK does not fit with the single cow /feed mill idea. If correct one would expect to see BSE clinically by the 2nd generation ie in those cattle that had eaten a relatively high dose of the infected batch of MBM from the feed mill.The feed would be likely to have produced a few cases on a susceptible farm, and thus should have been noticed (even in retrospect). There is no evidence that there were these isolated pockets of the disease prior to late 1984, Pitsham farm cases. BSE would have developed slowly in small areas with a lull throughout the lives of the second generation BSE cows before there was a second input of Prpbse into the food chain- likely to be 5 years minimum for incubation, slaughter, rendering, feed distribution and finally feeding to the next generation of cattle.One would expect to see an epidemiological picture that related to MBM from specific feed mills. There's no evidence for this.