BSE: the chemical connection
Dr Anthony and Benjamin Parish

What Doctors Don't Tell You, Nov 1998

Science has made a monumental blunder. Mad cow disease— bovine spongiform encephalopathy, or BSE—is not an infection spread by a pathogen, that is, a virus or a bacteria. It is a naturally occurring degenerative disease—a disease of old age— that is accelerated by toxic poisoning.

It all began with the sheep disease scrapie, which has similar symptoms to mad cow disease. Sheep staggered around and appeared to go crazy. But it was found that scrapie was not transmitted to other animals, and it was not thought to pose any threat to humans.

The mast likely cause of scrapie was massive chemical poisoning. Sheep are regularly dipped in chemical baths to kill off parasites. Their heads are invariably thrust under the surface and they often swallow some of the toxic dip.

For decades, sheep meat has been used to make cattle feed, with no ill effect. Problems only began in 1981 with changes in the meat-rendering industry. A non-solvent process was introduced. Previously, fat-soluble insecticides were literally dry cleaned out of the sheep meat. The same solvents used in dry cleaning—trichoroethylene and perchloroethylene— dissolved these harmful chemical toxins out of the food chain.

Unfortunately this change to the non-solvent process followed the warble-fly irradication campaign which lasted from 1978 to 1981. All sheep were compulsory dipped in an attempt to irradicate the parasite. This left additional neurotoxins in the fatty tissues, which the non-solvent rendering process did not adequately remove. Resulting toxin levels rose from around 5 per cent to some 7 to 14 per cent (Veterinary Record, March 2, 1991: 199-203). These toxins readily cross the blood-brain barrier (New Scientist, November 24, 1990: 53), causing spongiform diseases.

Indeed, Dr Gerald Wells, head of neuropathology at the Central Veterinary Laboratory in Weybridge, Surrey, told the BSE Enquiry in June: "The spongiform changes detected in the brains of cows were not in themselves conclusive and could have arisen from a variety of causes, including the ingestion of toxic substances." (limes, June 6, 1998)

The epidemic was further exacerbated by the fact that cow meat was also being rendered to make cattle feed. This enforced cannibalism essentially doubled up the toxic effect.

We have also discovered that BSE was not a new disease in cattle. In 1990, when we interviewed farmers in Norfolk about BSE, they said occasionally they had similar symptoms in older cows that had what they called the "jitters" or "jiggers". We believe that BSE is simply a disease of older cattle whose degenerative processes have been accelerated by poisoning so that it now affects cattle in their prime.

We see a similar relationship between Alzheimer’s disease and Creutzfeldt-Jakob disease (CJD). Alzheimer’s is a degenerative disease that results in memory loss in old age. CJD, we believe, is simply an acute form of the disease that occurs at a younger age.

Alzheimer’s is not a transmissible disease, but studies have shown that it can be induced (Proc Nail Acad Sci USA, July 1985; 13: 4898-901). CJD can also be induced. An experiment was unintentionally conducted on children with idiopathic hypopituitarism. They were injected with human growth hormones extracted from the pituitary glands of cadavers. Many have now developed CJD (New England Journal of Medicine, September 19, 1985: 728). This is a cause of what is known as protein poisoning.

Similar results were achieved when calves were fed with cow brain (Prion Diseases, Paris: Elsevier, 1996:51-6). The calves went on to develop BSE in all cases.

Scrapie cannot produce BSE. BSE cannot produce CJD (Prion Diseases). All three diseases have similar processes and, we contend, similar causes.

Indeed, if BSE is injected into other animals—cats, sheep, pigs, goats, monkeys—it does not produce a disease specific to that animal, which it would if it was transmitted by a pathogen. It simply produces BSE (Prion Diseases).

Here the animal receiving the injection is being poisoned not just by the original toxin but also by proteins produced in the course of the disease in the donor animal. Microscopic examination—of the recipient’s brain shows that the spongiform configuration depends on the donor species, not the species of the recipient—again, not a result you would expect if the disease was transmitted by a pathogen jumping species.

Since the beginning of the BSE epidemic in 1986, there have been close to 180,000 cases, mainly in the UK. Some scientists claim it is also widespread in Europe (Electronic Telegraph, June 17, 1996). The alleged pathogen is a protein that contains no DNA. It cannot be grown in tissue culture and does not appear to provoke an immune response. In other words, it is like no other pathogen ever seen before.

We contend that BSE and CJD can more readily be explained by the well known processes of poisoning. That means BSE cannot be transmitted and, thus, presents no threat to human health.

Dr Anthony and Benjamin Parish


Dr Anthony Parish is a Fellow of the New York Academy of Sciences. Benjamin Parish BSc is a Research Fellow.

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