Your response: from J.W. King

Do you represent a special interest group?
No

Comment:
The lack of proof that BSE and vCJD are not both caused by anticholinesterases

Paragraph 5 of the Review states 'the evidence that the vCJD epidemic is due to the agent (BSE, my insertion) via the food chain is still circumstantial.' This statement indicates that there is no concrete proof that the causative agent of vCJD is BSE-infected beef and indeed, therefore, the assumption that BSE has caused the vCJD epidemic may result in the disastrous side-tracking of a large amount of research effort and funding from investigations into the actual causes of BSE and vCJD. The hypothesis that vCJD was caused by eating beef (rather than by ingesting OP residues in various foodstuffs including vegetables such as carrots, lettuces, strawberries, apples and potatoes, samples of all of which have in recent years contained pesticide residues at dangerous levels - vide relevant MAFF publications) has never been validated.

The fact that there is no dietary link between BSE and vCJD has already been clearly established by the National CJD Surveillance Unit. The truth of the matter is contained in the Sixth Annual Report (1997) of the Unit in a highly relevant statement based on the following carefully-compiled evidence: 'The case-control study based on data from 23 cases of nvCJD and 19 age- and sex-matched hospital controls does not provide evidence of an increased risk in relation to prior medical treatment, occupation or diet' (my underlining). Table 17 of that Report shows that while 88% of the controls had eaten sausages, burgers or meat pies (probably containing MRM) more than once per week since 1985, only 80% of the nvCJD cases had done so.

It has never been proved that the agents causing either BSE or vCJD are not neurotoxic anticholinesterases such as organophosphates and carbamates. A wide range of anticholinesterases has been used in various head-lice treatments carried out on young people, and there has also been widespread use of various insecticidal sprays and other anticholinesterases in houses, greenhouses, gardens and public places.

Lorgue et al. [Lorgue G., Lechenet J and Rivière A.: Clinical Veterinary Toxicology, ed. in English by M.J. Chapman, Blackwell Science (1996) p.150] have stated that laboratory investigations of animals suspected of OP poisoning need to include measurement of acetylcholinesterase activity in the brains and plasma of carnivores and in the brains and whole blood of ruminants. They stress that brain samples when removed from dead animals must be frozen immediately in order to prevent degeneration of the enzyme.

This remark is in accordance with the following statements made during the hearing on Day 78 (5 November 1998) of the BSE Inquiry. The Transcript for that hearing contains the following exchanges:

(a)On p.44 of the BSE Inquiry Transcript:
PROFESSOR FERGUSON-SMITH: It (i.e. an organophosphate, my insertion) would have a central nervous system effect?

DR MARRS: Yes, sure, the medulla as well.

(b) On p.48 of the BSE Inquiry Transcript:

DR MARRS: In actual fact in most of those studies brain cholinesterase, the actual enzyme in the brain was measured, and it is usually that that is the critical end point.

MR WALKER: That would be turning to the CNS?

DR MARRS: The CNS, yes.

MR WALKER: What then was the conclusion in relation to the CNS?

DR MARRS: I think really as I have said that the effects are consistent with the only effect on the CNS being acetyl cholinesterase inhibition (my underlining).

There can be no doubt, in view of the statements of Lorgue et al. and Marrs quoted immediately ante that OPs lead to inhibition of brain acetylcholinesterase, and there is no doubt whatsoever (vide, per exemplum, Dulbecco [Dulbecco R.: The design of life, p.400]) that such inhibition would lead, via axonal degeneration, to cerebral necrosis of brain neurons. Dr Marrs, in fact, (vide pp.65 - 66 of the BSE Inquiry Transcript) when asked by Mr Walker if this would result in "some sort of damage to the brain cells, yes?" indicated that 'structural damage' would be caused in the brain. After this statement the following admissions were made:

MR WALKER: Which might give the appearance or in fact produce lesions?

DR MARRS: Yes. If you look under the microscope you will find neuronal cell necrosis, and that sort of thing.

PROFESSOR FERGUSON-SMITH: And spongiform change, astrocytosis?

DR MARRS: Astrocytosis you will get, yes (my underlining)…. It thus seems possible to the present author that the spongiform changes in the brains of cattle and humans (resulting in BSE and vCJD respectively) could be the result of exposure to anticholinesterases.
The similarities between the symptoms of OP poisoning and BSE

Pages 63 - 66 of the Transcript of Day 78 of the BSE Inquiry address the extremely important question of similarities which exist between the effects on the CNSs of cattle which have been exposed to OP poisoning and those which are suffering from BSE. It is apparent from these Transcript pages that both Dr Andrews and Dr Marrs were willing freely to admit that, because of the manner in which OP toxins act, there are many fundamental similarities between the symptoms of OP poisoning and BSE.

These important admissions, respectively from a leading veterinarian and from a toxicologist, have to be borne in mind and require careful consideration and evaluation when arguments are advanced by scientists (including the present author) who have concluded that BSE may be caused by the effects of anticholinesterase toxicity rather than by scrapie-infected MBM.
In view of the evidence presented ante, it cannot be claimed with any credibility (a) that BSE is not caused by anticholinesterases, or (b) that BSE and vCJD do not have a common cause viz. neurological effects associated with anticholinesterases.
Pages 63 - 66 of the Transcript contain the following exchanges:

MR WALKER: Thank you. Perhaps I could begin by asking a question of Dr Andrews as a veterinarian. Could I ask you first to comment on the difference between a bovine animal that has suffered from organophosphate poisoning and a bovine animal that has BSE?

DR ANDREWS: The first thing would be the duration of signs, I suppose, would be the first thing that would be different. If it is acute OP poisoning, it would only last literally hours or possibly a day or so. Of course, the signs would come on very rapidly and then decline. BSE is a very chronic disease, and the signs come on slowly, in most instances, rather than coming on very, very rapidly. So there would be a difference there.

There would be some signs that would definitely be relatively similar, because with the activity of OP toxicity, particularly the muscarinic activity, this is partially based on vagus; and some of the signs you appear to get with BSE, again, appear to be vagal involvement (my underlining).
So, things like a constriction restriction of the pupil, reduction in ruminal movements, reduction in appetite and so on would be similar to both.

Other signs, particularly with BSE, now a lot of the cases I would see you had a very marked apprehension in the animal. It is almost as if their consciousness,what they saw and what they were interpreting what they saw were different; and they became very worried because of that. It seems they had an apprehension which became worse; and I think this is partly why one got the apparent aggression later on with some of these animals.

Muscle twitches, again, you would see in both. Ataxia or wobbliness and incoordination you may see in both. Again, both animals might actually go down to the ground. Again, that would depend on the OP activity and where that was. A lot of the signs would be not dissimilar (my underlining).
The problem is that anything affecting the nervous system, that is central anyway, is going to have really two activities. One would be increased activity or one is depression. How much of that and where the actual area affected will then depend on what signs you get. Obviously BSE does affect part of the area of the brain which is similar to where the vagus comes off, which is this parasympathetic nerve.

MR WALKER: Could I ask, can organophosphate poisoning lead to lesions in the brain (my underlining)?

DR ANDREWS: I honestly do not know the answer to that question. It does effect the brain, yes.

MR WALKER: Dr Marrs?

DR MARRS: Presumably by "lesions" you mean structural lesions, structural damage.

MR WALKER: Some sort of damage to the brain cells, yes?

DR MARRS: The received wisdom is that mild or moderate or even quite severe organophosphorus poisoning is totally reversible if treated properly; but certainly if you give experimental animals doses near to the lethal dose, where you get convulsions, you can produce structural damage.

MR WALKER: Which might give the appearance or in fact produce lesions?

DR MARRS: Yes (my underlining). If you look under the microscope you will find neuronal cell necrosis, and that sort of thing.

PROFESSOR FERGUSON-SMITH: And spongiform change, astrocytosis?

DR MARRS: Astrocytosis you will get, yes.
Author';s Note: Readers are asked to excuse the fact that one or two of the sentences from the BSE Inquiry Transcript quoted immediately ante were also reproduced on an earlier page of these comments; this was done deliberately in order to emphasise the extreme relevance of the topic under discussion.

Paragraph 7 of the Review: The reasons why cats, cattle and deer have developed spongiform encephalopathies, but dogs and horses have not

It was clearly admitted by the relevant witnesses at the BSE Inquiry Hearing on 5 November 1998 (vide pp. 67 - 70 of the Transcript for that day) that different species have - as a result of different enzymatic processes in their livers - different abilities to detoxify themselves after intoxication by xenobiotic compounds, and it was accepted that the inability of cats to produce glucuronide in their livers would be a reason why cats possessed a poor detoxification capability. The present author’s statement referred to on p.67 of the Transcript originates from Oehme [Oehme F.W.: Agricultural and veterinary toxicology of anticholinesterases in Clinical and experimental toxicology of organophosphates and carbamates ed. by B. Ballantyne and T.C. Marrs, Butterworth Heinemann (1992)] who drew attention to the relative inability of cats (specifically as opposed to horses and dogs) to detoxify themselves.

Data published by Lorgue et al. [Lorgue G., Lechenet J and Rivière A.: Clinical Veterinary Toxicology, ed. in English by M.J. Chapman, Blackwell Science (1996)] establish very clearly that the LD50 doses for cats are in general very much smaller than those for other species - especially dogs - and it is suggested by the present author that this deficiency on the part of cats is the reason why many cases of FSE have occurred in the UK whereas, as far as he is aware, there has not been a single verified case of spongiform encephalopathy in a dog anywhere in the world.
Both cats and dogs have worn carbaryl-impregnated flea collars manufactured by Johnson’s Veterinary Products Ltd. (Carbaryl is, as its name suggests, an anticholinesterase carbamate.) Whether or not cats developed FSE from these collars is not known with certainty, but it is clear that no dogs died as a result of wearing them.

Another dangerous systemic anticholinesterase which was used as a "spot-on" for treating both dogs and cats for fleas was diazinon in the form of the compound Droplix. It is widely known that this compound was withdrawn from use after a significant number of cats had died following Droplix applications; as far as the present author is aware, no dogs died following Droplix applications. The different responses of cats and dogs to the use of Droplix supports the suggestion that the inability of cats to detoxify organophosphates led to FSE while dogs have not developed any form of spongiform encephalopathy.

It is relevant to note that, although dogs have been treated for ticks using sponge applications of phosmet in a systemic formulation, none of them developed spongiform encephalopathy as a result; it will be shown elsewhere in this Section that in general the LD50 doses of anticholinesterases are substantially greater for dogs than they are for cattle, and this fact may provide an explanation of why the pour-on use of systemic phosmet compounds could have led to BSE in cattle whereas sponge applications of phosmet did not result in spongiform encephalopathy in dogs.

Apart from the carbaryl-impregnated flea collars referred to ante, fenitrothion, another organophosphate insecticide, was also used in a systemic form (Tiguvon) as a "spot-on" treatment for fleas on dogs and cats (vide document supplied by MAFF in 1998).

A paper by Bell et al. [Bell T.G., Farrell R.K., Padgett G.A and Leendertsen L.W.: Ataxia, depression and dermatitis associated with the use of dichlorvos-impregnated collars in laboratory cats, JAVMA 167 No.7, pp.579 - 586, (1 October 1975)] has described the deadly effects of dichlorvos-impregnated flea collars on cats; the abstract of this paper showed that 10% of the cats which were fitted with dichlorvos-impregnated collars actually died during the test period; as far as the present author is aware, no dogs have ever died as a result of wearing dichlorvos flea collars.

The paper by Bell et al. referred to ante quotes (in the right-hand column of p.585 of their paper) the fact that "in the cat, erythrocyte ChE (i.e. acetylcholinesterase) activity is 2% of that in man ….". This result was established by Callahan and Kruckenberg [Callahan J.F. and Kruckenberg S.M.: Erythrocyte cholinesterase activity of domestic and laboratory animals: normal levels for nine species, Am. J. Vet. Res. 28 No.126, pp.1509 - 1512 (September 1967)]. Table 1 of that paper, on p.1510, shows that the erythrocyte cholinesterase activity of cats is only 2% of that of man whereas, in agreement with Oehme’s general statement referred to ante, dogs exhibit erythrocyte ChE activity equal to 7.7% of the normal level of man while the level in horses is 11.7% of that of man. The acetylcholinesterase activity levels in dogs and horses are therefore respectively about 4 and 6 times the rate of that in cats. These results offer a ready explanation of why neither dogs nor horses developed spongiform encephalopathy from normal exposure to anticholinesterases.

As Callahan and Kruckenberg (loc. cit.) wrote in the first paragraph of their paper, acetylcholinesterase activity "is also useful in toxicologic studies of anticholinesterase materials". Obviously information about the LD50 levels of various organophosphates and other toxins for different species provides excellent indications of the relative susceptibility of the different species involved to damage by the relevant compounds. A cursory study of the data contained in Lorgue et al. (loc.cit.) shows that, in addition to cats, another species with very low LD50 or LD levels is cattle. Cattle have, on average, very much lower lethal dose levels than, for example, dogs and this fact lends support to the argument that BSE is a result of exposure to OP poisoning.

Cattle in Great Britain could have been exposed to anticholinesterases by any of several different routes:

(a) Before 1988 MBM included sheep which had died after dipping. As was discussed on p.28 of the BSE Inquiry Transcript, such animals would have had the toxic OP used in the dipping process perfused throughout their whole bodies.

(b) The use of OP fly sprays as "housing sprays" in buildings entered by cattle - vide p.19 of the BSE Inquiry Transcript.

(c) The use of OP warblecides which, as is well known, were particularly widely used in Great Britain (but not in Northern Ireland) during the years 1978 - 1982. Even though the number of warble fly attacks may have decreased after that date, it is not necessarily correct, as suggested on pp.85 - 86 of the Transcript, that OP warblecides would have been much less used in later years. MAFF document PB2164 published in 1995 urged that "all farmers (my underlining) in Great Britain should seriously consider treating their cattle this autumn".

Farmers are obviously likely, just as any other group of individuals would be, once they have discovered something relevant to their work which acts efficiently, such as a particular organophosphate warblecide, to continue to use it. It seems worth speculating whether the campaign by MAFF to persuade farmers to use warblecides throughout Great Britain in 1995 may have accounted for the unexpectedly large number of BABs which have developed BSE. BABs are cattle which, although born long after the 1988 ban on the inclusion of ruminant protein in cattle feed, have unexpectedly developed BSE.

The MAFF BSE Enforcement Bulletin Issue No. 27 (October 1998) shows that, by 15 October 1998, there were 37,187 BABs, i.e. a staggering and inexplicable 22% of the total number of BSE cases which had occurred in Great Britain since 1988. The present author believes that the occurrence of further cases of BSE will not cease until all avenues by which cattle are exposed to anticholinesterases are closed. In any event, systemic phosmet pour-ons were also used for treating lice in cattle, and it is not clear that this practice ceased when warbles were eradicated after about 1982. (It should be appreciated that the OTMS and other slaughter programmes will result in a decline in the number of cases of BSE, simply because all the cattle likely to develop the disease have been slaughtered; this does not prove, unfortunately, that once the various slaughter programmes have stopped, the disease will have disappeared permanently.)

(d) The use of organophosphate chemicals to spray arable crops (vide pp.19 - 20 of the BSE Inquiry Transcript) some of which were no doubt used in cattle feed. The BSE Inquiry was told earlier by cattle feed manufacturers that no tests were carried out on the OP content of cattle feed because such information was not required by the UK authorities. The WHO [Environmental Health Criteria series No.124 (1991), p.53] and MAFF [MAFF/HSE Annual report on pesticide residues containing data for 1987 and 1988] have published information showing that UK cattle feed contained, throughout the whole period 1982 - 1988 (which were significant years in relation to the BSE epidemic), residues of the dangerous organochlorine lindane at levels above, and in fact up to 11.5 times, the legally permitted MRL.

It appears unlikely that anybody will now ever be able to establish what residues of the many different anticholinesterase compounds which were used on the various components of cattle feed actually appeared in the feed. MAFF has shown that, apart from the appalling situation referred to ante in which whole cattle feed contained residues at illegal levels, individual components of cattle feed (such as cottonseed) used in the UK in 1992 and 1993 sometimes contained residues of lindane greatly in excess of the legal limit.

(e) It is well known that pasture is sprayed with anticholinesterases in order to destroy weeds and various crop-damaging pests, and that cattle may thereafter be allowed to graze on contaminated pasture.

It has been established in this Section that cats and cattle suffer from much higher susceptibility to poisoning by organophosphates and other toxins than do horses and dogs. Lorgue et al. (loc. cit., p.149) have indicated that ruminants (which include all the various types of deer and antelopes as well as cattle, sheep and goats), birds and cats suffer from lengthy and, presumably therefore inefficient, detoxification processes. It is therefore hardly surprising, in view of the fact that organophosphates have been fed to, or used on or used to clean the living spaces of various species of zoo animals, that certain types of animal, which are ruminants with inefficient detoxification systems, have developed spongiform encephalopathies. The fact that large proportions of the wild bird populations in Great Britain appear to have disappeared in recent years may also be explained by the agricultural use of organophosphates.

A report from the USA [BBC Ceefax (4 December 1997)] indicated that some wild deer in the USA are suffering from BSE; those deer have never been fed MBM (and so have certainly never ingested scrapie-infected feed), but they have, apparently, been exposed to organophosphates. The report concluded that the "BSE has been caused by pesticides and not (by) infected animal feeds" (my underlining).

It was stated (vide p.18 of the BSE Inquiry Transcript) that the formulations of anticholinesterases used in dipping sheep are not systemic. This statement appears to be inconsistent with the regulation quoted by MAFF to the effect that sheep that have been dipped are not permitted to enter the human food chain for up to 42 days after dipping. This regulation is in line with p.30 of the Transcript in which it was conceded that phosmet used as a pour-on remains inside a cow’s body such that after fourteen days there was still some persistence ("It would still have been present in tissue" but not, apparently, at a level high enough to kill lice). A situation in which an anticholinesterase is present throughout a cow’s body (including, no doubt, its brain) for several weeks seems highly undesirable in view of the fact that 'All parasiticides will have some effect on the host" (vide Transcript p.15).

Pages 66 - 71 of the BSE Inquiry Transcript contain the following exchanges:
PROFESSOR FERGUSON-SMITH: In these cases is the histopathology distinguishable from spongiform encephalopathy?

DR MARRS: I do not think I am qualified to answer that question.

MR WALKER: Another aspect of what happens in the cow. As I understand it, in terms of detoxifying the effects of pesticides it is a question of having the right enzymes in your liver; is that right, or is that an oversimplification?

DR ANDREWS: It is fair simplification. It is not just that, but it is a fair simplification. Yes.

MR WALKER: Does that vary from species to species?
DR ANDREWS: The answer is, as far as I am aware, yes.

MR TASKER: That is right.

DR MARRS: Yes, it does.

MR WALKER: I have seen a suggestion that in particular in cats it may be more difficult to deal with organophosphates than in other animals.

DR ANDREWS: I think that would be fair (my underlining). I think each species has a different activity, and therefore cannot be considered to be the same as another species.

MR WALKER: Thank you. Our bundle contains a statement from Dr King where he has drawn attention to the inability of cats to produce something called glucuronide, if I have the pronunciation correct. Are you able to comment on that, Dr Andrews?

DR ANDREWS: I think the toxicologist would be better qualified to comment on it.

MR WALKER: Have you a comment on that?

DR MARRS: Again, it is not really my area of expertise, but I have a bit of general knowledge on the subject which might be helpful. Glucuronidation is one method of excreting toxic chemicals from the body; and cats are notorious for the fact that they do not do it very much (my underlining). It is typical of the way cats deal with a lot of xenobiotic compounds.
And also the following:

DR ANDREWS: Could I just come in on a slightly different tangent on this? Organophosphorus compounds have been used in cats very successfully, actually, for treatment of ectoparasites. It is also fair to say, not being a toxicologist but looking at what can go wrong, is organochlorides were not used in cats because of their potential for toxicity compared with dogs and so on. So they tended not to be used in that species, going back to the same type of reasons.

MRS BRIDGEMAN: You said cats were notorious for this sort of weakness. Are there any other animals that in that same category, which you do not use because their livers give up or whatever they do?

DR ANDREWS: I do not think the livers give up. There is one pathway, which is not available to them.

MRS BRIDGEMAN: Forgive my usual simplicity.

DR ANDREWS: How Dr King has derived what he is thinking is that I wrote a paper many years ago now about side effects from organophosphorus compounds. Again, I did have access to confidential data from all the companies and the manufacturers, the distributors and manufacturers. What I found quite interesting in that is that in quite a few cases where there was a problem it was not an individual problem but it was a group problem on that. Now, that could have been because of overdosing or some other reason for that. In some instances, it definitely did look as though they had some metabolic compromise. By that I mean perhaps some compromise of their livers, and their ability to detoxify; and that may have had an effect, which is it is an indirect way, again, of saying that – or agreeing with you that the liver is very, very important.

MRS BRIDGEMAN: So the simply "yes" to my simply question. We are interested because we have observed that the problem, that BSE transfer has taken place in certain kinds of animal; the cat is one example. That was why I wondered -- mink is another. I wondered well these were this sort of group that were susceptible in this kind of way?
And the following:

MRS BRIDGEMAN: Before we turn to that point I still do not have the answer to the point I put. Maybe the veterinarian is the best person to give an observation. Are the classes of this animals that have this particular susceptibility in any way match perhaps what we have seen as the target animals with transferable encephalopathies?

DR ANDREWS: The answer is that I do not know the answer actually. One can see some of the species where there is that susceptibility. You may make a very good point. Mink might be a very suitable model (my underlinings)…..

Table 1 of Paragraph 7 of the Review: The possible origin of Kuru in man

The FSA Review includes Kuru in the list of TSE diseases experienced by man, but consideration must be given to the geographic origin of that disease. A very important concept about chronic ill-health which materialises decades after exposure to neurotoxins is introduced on p.54 of the OTA book [U.S. Congress, Office of Technology Assessment: Neurotoxicity: Identifying and controlling poisons in the nervous system (1990)]; this is described in the paragraph which reads:

'Naturally occurring toxic substances can also affect the nervous system. An unusual combination of the neurodegenerative disorders ALS, Parkinson's disease, and Alzheimer's disease endemic to Guam (known as Guam ALS-Parkinson's dementia) puzzled investigators for many years because of the correlation between incidence of the disease and preference for traditional foods. During food shortages, residents of the island ate flour made from the false sago palm, a member of the neurotoxic cycad family. The cycad contains one or more naturally occurring toxic substances that appear to cause a neuromuscular disease in cattle and trigger slow degeneration of neurons (my underlining).

As old age approaches and natural brain cell death accelerates, the effects of the degeneration become apparent and the neurological symptoms appear. This possible link between a naturally occurring compound and a neurodegenerative disease has stimulated the search for other toxic substances that may trigger related neurological and psychiatric disorders. This work and that of others led to the hypothesis that Alzheimer's disease, Parkinson's disease, and ALS could be due in part to damage to specific regions of the central nervous system caused by environmental agents and that the damage may not become apparent until several decades after exposure.'

It is worth noting here that Papua New Guinea, where Kuru occurred (and presumably first started in a particular individual in a particular family), is located in that part of the world densely populated by cycad trees; the above paragraph from the OTA book, and especially the statement that "The cycad contains one or more naturally occurring toxic substances that appear to cause a neuromuscular disease in cattle and trigger slow degeneration of neurons" (my underlining), appears to the present author to be highly relevant not only to the origin of Kuru but also to the BSE/vCJD problems with which Britain is at present struggling. (The toxic cycad flour is of course of no relevance to BSE or vCJD, but the present author believes that other neurotoxins such as anticholinesterase pesticides could be of fundamental relevance to these diseases.)
Paragraph 10 of the Review: The similarity of the "biochemical fingerprints" of BSE and vCJD

It has been indicated ante that at the Hearing of the BSE Inquiry on Day 78 relevant experts admitted that the symptoms of OP poisoning and of BSE are similar. If, as the present author has suggested, both BSE and vCJD are the result of neurological damage following neurotoxic effects produced by anticholinesterases, then it would not appear to be particularly surprising that the "biochemical fingerprints" of vCJD and of BSE bear a close resemblance to one another. The present author would suggest that, far from this resemblance proving that BSE causes vCJD, the resemblance rather suggests that both diseases have a common origin, viz. a neurological assault following the ingestion of anticholinesterases.

Paragraphs 15 and 16 of the Review: The scale of the vCJD epidemic

Theoretical estimates of the size of the vCJD epidemic, calculated on the assumption that all the cases will be caused by BSE, lie between a couple of hundred and 136,000. The present author believes that the epidemic of vCJD (and BSE for that matter) would be much smaller and would end much more quickly if the use of organophosphates and other anticholinesterases was greatly reduced and, in fact, strictly controlled or banned wherever possible.

In human terms (and also, for that matter, in animal terms) the use of alternative agricultural chemicals instead of anticholinesterases would probably be significantly more cost-effective (if such neurotoxic chemicals were shown to be the cause of vCJD) than allowing the vCJD epidemic to continue until perhaps 136,000 people have died of the disease.

Paragraph 23 of the Review: The possible effect of anticholinesterases present in dipped sheep where carcases were included in MBM

The FSA Review states that "….the major route of transmission of BSE in cattle was through …. ruminant-derived MBM in animal feed". These words quoted may well be completely true, but this fact does not establish that the origin of the disease was scrapie-infected sheep. In the opinion of the present author, the original cause of BSE is equally likely to have been the inclusion in animal feed of the carcases of sheep which had died following dipping in organophosphate-