Day 16====page 50
1 deficiency, contact with both
potash-rich fields and wet
2 weather exacerbated Birthday's symptoms. Total
3 remission of her symptoms was induced 36 hours after
4 subcutaneous injection of the first bottle of magnesium
5 sulphate. Symptoms returned moderately by early June
6 and MAFF vets who were called in diagnosed early stage
7 symptoms of BSE, issuing a Form A BSE Suspect Notice on
8 the cow. Further treatment with two bottles of
9 magnesium sulphate induced total remission once again,
10 and at the beginning of September, MAFF vets withdrew
11 the BSE notice altogether."
12 I close the quote there. What I would like to do
13 is to just take you to some of the correspondence that
14 had occurred at this time. Before I do, can I confirm
15 by this time you had moved to High Barn Farm?
16 MR PURDEY: Yes, this was all on High Barn Farm, all this.
17 MR WALKER: The first letter I want to take you to is in
18 July 1991. We have it in the year books for 1991. The
19 year book for 1990 can go away. Hold on to the article,
20 because we will come back to that.
21 In YB 91, if you go into tab 7. There is rather a
22 lot in our 1991 year book. We are going to have to
23 divide it into two, I think, quite soon. I think the
24 first document after tab 7 is a letter dated 14th July
25 1991. It is sent from you to the Chief Veterinary
1 Officer at MAFF. Is that right?
Is this a copy of a
2 letter that you sent?
3 MR PURDEY: Yes, that is right.
4 MR WALKER: In paragraph 1, you describe what had happened
5 to Churnside Birthday:
6 "Over the last two or three months, this cow
7 started to develop what appeared to be a chronic
8 staggers type of disorder, which was partially rectified
9 after administering magnesium sulphate into the cow.
10 However, after blood tests were taken for magnesium, et
11 cetera, no mineral deficiency could be identified within
12 the cow, and my vets are now considering that this cow
13 is afflicted with BSE, and will be contacting
15 Then you go on to describe your keen interest in
16 environmental toxins. You say a bit about the
17 conception that exposure to neurotoxicants upsets the
18 cow's immunological equilibrium. In the third paragraph
19 you say:
20 "If your vets endorse my vet's verdict of BSE,
21 I would like to attain some form of guarantee from
22 yourselves before I hand over the afflicted cow that
23 I may be granted independent access for examination of
24 CNS tissue."
25 On the last paragraph of this page, you go on to
1 outline various correlations
which suggest why BSE could
2 be a sequel to an acute or chronic neurotoxicant
3 disorder some years earlier to the surfacing of the
4 outward symptoms.
5 What I would like you to do is to take you to some
6 of the things you have said about those correlations, if
7 I may? Is that all right?
8 MR PURDEY: Yes.
9 MR WALKER: Just over the page you refer to some cattle
10 herds within the UK, as well as all herds within some
11 other countries, having consumed the alleged prion
12 contaminated feeds, yet remaining completely devoid of
13 BSE outbreak to date.
14 MR PURDEY: Yes.
15 MR WALKER: Then the following paragraph, you refer to the
16 fact that in your own farm you had not used the systemic
18 After that you go on to refer to the fact that
19 registered organic herds may well have fed the cake in
20 the 20 per cent that was bought in the cake allowance
21 previously permitted by the Soil Association standards.
22 Then you refer to the point about use at London
23 Zoo, and pet cats which, we had seen earlier. Then you
24 turn to journals which showed that certain environmental
25 toxins, such as aluminium and anti-thiamine agents, and
1 some others, had increased
permeability of the
2 blood-brain barrier, and had disrupted the -- is that
4 MR PURDEY: Yes, pinocytotic vesicles.
5 MR WALKER: -- pinocytotic vesicles in the vessel walls. I
6 was interested there that some of the things that you
7 referred to, they included not only anti-thiamine
8 agents, radiation, anaesthesia, but also cycad nuts.
9 MR PURDEY: Yes.
10 MR WALKER: I think this was a study on Guam?
11 MR PURDEY: Yes, Guam, yes, that is right. A very
12 interesting study.
13 MR WALKER: You referred to various general articles. I
14 think what happened on Guam had been the subject of a
15 book by Oliver Sachs, had it not, called "Island of the
16 Colour Blind"?
17 MR PURDEY: This was the first milestone in accepting the
18 role of chemicals, albeit it naturally-occurring, in the
19 triggering off of well-known neurological diseases like
20 Alzheimer's, which is very similar to TSE, and
21 Parkinson's and motor-neurone disease. So to me this
22 was very interesting research that I homed into right
24 MR WALKER: I think the disease on Guam was called lytigo
1 MR PURDEY: It was called
something like that, yes.
2 MR WALKER: It was studied by Professor Gajdusek whom we
3 know did some studies into kuru and other aspects of
4 spongiform encephalopathy?
5 MR PURDEY: Yes, and Peter Spencer as well, who did a lot
6 of work.
7 MR WALKER: Having referred to that, you went on to a
8 demonstration that anti-cholinesterase chemicals had
9 overdriven the regions of the digestive tract that were
10 intensively supplied with cholinergic receptors. Then
11 you went on to refer to research teams investigating the
12 delayed neurotoxicity of certain anti-cholinesterases
13 and reported spongiosis.
14 Over the page, you refer to the work by Bouldin
15 and Cavanagh that we mentioned earlier on this morning.
16 Then about halfway down that page in a paragraph --
17 perhaps I should read the whole paragraph:
18 "Other dairy farmer colleagues of mine also report
19 that their diagnosed cases of BSE temporarily responded
20 dramatically to magnesium and calcium treatment.
21 Interestingly, these same mineral deficiencies were
22 considered along with chemical neurotoxins to be the
23 essential prerequisites for triggering the Guam
24 syndromes. The very fact that some of the BSE symptoms
25 are reversible suggests that not all symptoms can be
1 accountable to the direct
physical damage created by the
2 infective prion agent. Perhaps hyperparathyroid
3 activity is involved here as a sequel to exposure to
4 chemical neurotoxins well known for overdriving the
5 neuroendocrine system."
6 Then you went on to say that in research trials on
7 the Guam degenerative disorders and the Birmingham
8 research into anti-cholinergic effects, it showed that
9 it was apparent that there were similar pathological
10 duplications involved in the BSE syndrome, and finally
11 suggested that whether it was a question of identifying
12 the neurotoxic trigger or eliminating one, doing the
13 necessary research would be an advance into
14 comprehension of slow viral encephalopathies with
15 knock-on benefits for public health at large?
16 MR PURDEY: Yes.
17 MR WALKER: There are a number of references in this
18 letter. How long did it take you to prepare this
20 MR PURDEY: I do not think this is very long, not compared
21 to this article, burning the midnight oil for many
22 nights, many nights.
23 MR WALKER: Thank you. You tell us in paragraph 8 that
24 Mr Meldrum replied to you on 25th July 1991 saying that
25 the Department could not grant you independent access
1 for examination of central
2 Unfortunately, we have not been able to locate a copy of
3 that letter at the moment. Can you recollect whether he
4 dealt with the points that you were making about the
5 correlations between BSE and these other diseases?
6 MR PURDEY: No, no. No.
7 MR WALKER: You cannot recollect that?
8 MR PURDEY: No, he did not. He just answered the fact that
9 I could not have central nervous system tissue.
10 SIR NICHOLAS PHILLIPS: Did he explain why?
11 MR PURDEY: He just said that it was against -- you know,
12 the law was that it could only be analysed in Government
13 laboratories. It was MAFF property. Once the cow was
14 taken under a BSE order, it became MAFF's property,
15 and ...
16 SIR NICHOLAS PHILLIPS: That would not explain why MAFF
17 could not release a bit of the cow back to you if it
18 wanted to.
19 MR PURDEY: Well, exactly.
20 SIR NICHOLAS PHILLIPS: But no explanation was given other
21 than it was their policy not to do so?
22 MR PURDEY: Yes, that is right.
23 SIR NICHOLAS PHILLIPS: I see.
24 MR WALKER: I would like to finish off this bit of the
25 story before we break for coffee. If we go on to tab 11
1 in our bundle, the second
document behind tab 11, our
2 reference is YB 91/11.13/1.1. Do you see there a letter
3 dated 13th November 1991 from the Taunton office of the
4 Ministry of Agriculture, Fisheries and Food. The
5 veterinary officer is writing to you and your wife at
6 High Barn Farm. Is that a letter you received?
7 MR PURDEY: Yes.
8 MR WALKER: This letter says:
9 "As you are aware, the brain of your bovine
10 animal ...", the cow, "... identification number
11 JB122-178 ...", which I think is Churnside Birthday,
12 "... was collected for examination following slaughter
13 on 29th September 1991. The examination was intended
14 solely to confirm whether or not the animal was
15 suffering from bovine spongiform encephalopathy and no
16 attempt could be made at providing a differential
18 Can you tell the Committee what that means, that
19 no attempt had been made to provide a differential
20 diagnosis, or what did you understand it to mean?
21 MR PURDEY: I suppose that meant that they had not looked
22 at any other possibility; that all they were looking for
23 was whether it was BSE positive or not. There was this
24 phenomena of BSE negative, where some cows were coming
25 back that had been taken under the BSE order, exhibiting
1 the symptoms of BSE, and were
coming back BSE negative.
2 There were one or two publications in the Veterinary
3 Record, for instance, about BSE negative.
4 MR WALKER: By that, you mean the number of cattle that had
5 been assessed by a vet as likely to be suffering from
7 MR PURDEY: Yes.
8 MR WALKER: And that had led to them being slaughtered under
9 the slaughter policy?
10 MR PURDEY: Yes.
11 MR WALKER: Then, when examination of the head took place,
12 the information led to the conclusion that this cow,
13 while it had shown the symptoms of BSE, did not in fact
14 suffer from that disease?
15 MR PURDEY: Yes, that is right. I think it did not show
16 the ballooning vacuoles, the swelling of the brain. But
17 it could have just been at an earlier stage of the
18 disease and had not yet demonstrated that kind of
20 MR WALKER: The interesting question is exactly what the
21 animal was suffering from if it had not shown the
22 lesions characteristic of BSE.
23 MR PURDEY: Yes.
24 MR WALKER: What you were then told, in the second
25 paragraph, was that they had received the result of the
1 laboratory examination, and that
lesions consistent with
2 BSE were in fact identified with the result that the
3 disease is therefore confirmed in that animal.
4 I would just like to take you back to the --
5 PROFESSOR FERGUSON-SMITH: Can I interject and ask: I just
6 wonder if that letter says, "We were not excluding any
7 other form of spongiform degeneration which could have
8 had a toxic effect"?
9 MR PURDEY: Yes.
10 PROFESSOR FERGUSON-SMITH: He was covering, is that right?
11 MR PURDEY: I did not think that, but now, yes, that is a
12 possibility. Yes.
13 MRS BRIDGEMAN: If I may make a comment? This strikes me
14 as a standard letter into which they have inserted your
15 address and your bovine animal number, so it can apply
16 universally; but that is perhaps something that we can
18 MR WALKER: I wanted to take you back, to finish off the
19 story, by looking at your article again which you have
20 loose, I think, just there.
21 MR PURDEY: Yes.
22 MR WALKER: On page 69, if you look at the course of events
23 there, we have reached the third to last paragraph on
24 page 69 of the Nutritional Medicine article. There you
1 "Despite the fact that the
2 symptoms of the early stages of BSE never recurred,
3 Birthday started to lose weight, her muscles atrophied,
4 she developed a dejected appearance, and on
5 September 29th when an extreme bout of wet weather set
6 in, she collapsed in a muddy gateway and was unable to
7 rise. MAFF vets were called in, who instantly reimposed
8 the BSE notice and slaughtered her. Her post-mortem
9 revealed BSE positive lesions."?
10 MR PURDEY: Yes.
11 MR WALKER: Just to conclude, the story is of a cow that
12 exhibits some symptoms which might be attributed to BSE,
13 but then recovers from those after dosing with
14 magnesium, only later on to display the symptoms again
15 and eventually to need to be slaughtered?
16 MR PURDEY: Yes.
17 MR WALKER: Well, I am going to come on, after the coffee
18 break, to the article you then wrote in The Ecologist
19 describing what happened. Perhaps if we might break for
20 coffee now. Would that be convenient?
21 MR PURDEY: Yes.
22 MR WALKER: We will resume in about 20 minutes.
23 (11.05 am)
24 (Short break)
25 (11.30 am)
1 MR WALKER: I think I said after
coffee I would take you to
2 the article in The Ecologist. Perhaps we could
3 distribute that? We have an article entitled "Mad Cows
4 and Warble Flies: A Link Between BSE and
5 Organophosphates?" I think this is published in volume
6 22 of The Ecologist, in their issue for March and April
7 1992; is that right?
8 MR PURDEY: Yes.
9 MR WALKER: In this article, I think you begin by describing
10 the suffering of Churnside Birthday.
11 MR PURDEY: Yes.
12 MR WALKER: After having described the way in which she was
13 put down, at the end of the third paragraph you say:
14 "All the pleas made to MAFF for various
15 post-mortem neuropathological explorations were rejected
17 A. Yes.
18 MR WALKER: Then you say a little bit about the prion theory
19 and BSE negative cows that we discussed earlier.
20 MR PURDEY: Yes.
21 MR WALKER: Then, under the heading "Genetic and
22 Environmental Factors", you say:
23 "Much of the scientific establishment seems to be
24 ignoring the importance of the genetic and environmental
25 factors which influence slow virus diseases."
1 MR PURDEY: Yes.
2 MR WALKER: Then you refer to some things which you say
3 need investigating, in the final paragraph on that page.
4 You refer to large differences in the incidence of BSE
5 between different herds and the geographic differences
6 in the spread of the disease.
7 MR PURDEY: Yes.
8 MR WALKER: Then we have a section which is entitled "The
9 Organophosphate Link". You begin by saying:
10 "A striking feature of BSE epidemiology in Britain
11 is that the epidemic is at its most intensive in the
12 areas which were designated by MAFF as 'warble fly
13 eradication zones' approximately three years
15 I think that we will come on to the more detailed
16 explanation that you give of that in the article in
18 MR PURDEY: Yes.
19 MR WALKER: Just while we are dealing with it here in The
20 Ecologist, in the next sentence you said:
21 "All farmers were legally obliged to treat their
22 cattle with one of three pouron quasi-systemic
23 'phenylphosphorothioate' types of organophosphorous
24 insecticide known as phosmet, famphur and Fenthion."
25 At this stage, was it still possible to use
2 MR PURDEY: Oh yes, yes.
3 MR WALKER: There was the possibility then of using
4 something other than an organophosphorous?
5 MR PURDEY: Well, really only on beef cows, unless you
6 wanted to bankrupt your business by throwing milk away
7 for 28 days.
8 MR WALKER: I think that most of the points that you
9 describe in this section are points that we have covered
10 already, references to the zoo and cats and so on.
11 I was going to take you on to the next section
12 headed "Neurological Effects of OPs". This is the
13 middle column on page 53. You say there that:
14 "Acute poisoning by organophosphates causes the
15 nerves to go into 'overdrive' due to the excessive
16 release of acetylcholine at the synapses (nerve
18 You talk about the neurotoxic effect. At the
19 bottom of that column, you say:
20 "The pattern through which the nerves degenerate
21 in these victims of OP precisely duplicates several
22 types of motor neurone diseases such as Friedrich's
23 Ataxia and amyotrophic lateral sclerosis."
24 You draw attention to some work that has been done
25 in that regard.
1 Then, having done that, at the
foot of the
2 right-hand column on page 53, you say:
3 "An important link between the slow viral
4 encephalopathies (such as scrapie and BSE in animals,
5 and kuru and CJD in humans), and the human 'non-viral'
6 degenerative diseases (such as Parkinson's, motor
7 neurone and Alzheimer's disease) is suggested by the
8 similar way in which all these diseases develop."
9 Then you go on to describe the ways in which they
10 show the clinical symptoms over time. Then the next
11 section of the article is headed "A Reduced Capacity for
13 You say in the left-hand column on page 55 that:
14 "There is evidence that there may be a reduced
15 capacity for detoxification in the BSE cow due to a
16 deficiency of calcium and magnesium."
17 I wonder if you could describe that evidence a
18 little to the Committee?
19 MR PURDEY: That would be some of the detoxification
20 enzymes that are involved in breaking down chemical
21 pathways, when they are detoxifying are actually
22 activated. There are cofactors in enzymes that are
23 often minerals or vitamins, for instance, and magnesium
24 certainly plays a role in the degradation in activating
25 enzymes involved in these detoxification pathways. But
1 I think it goes a lot further
than that, my current
2 thinking, you know, there are many more things.
3 SIR NICHOLAS PHILLIPS: That sounds more like that there is
4 a theory rather than there is evidence?
5 MR PURDEY: There is evidence, yes. Magnesium is involved
6 in activating certain enzymes in the detoxification
7 pathways from ...
8 MR WALKER: I think the evidence that you refer to here are
9 some of the things that you have seen in your own herd,
10 the symptoms appearing and then the effect of treatment
11 with magnesium?
12 MR PURDEY: It would be referring to both observations in
13 my own herd and then relating that to the published
14 scientific literature, various articles that cited the
15 role of magnesium, for example.
16 MR WALKER: I was interested by the right-hand column on
17 page 55, where you say:
18 "In response to a letter of mine pointing out this
19 magnesium connection, the head of MAFF's BSE
20 Epidemiology Unit, John Wilesmith, stated that in MAFF
21 trials, therapy with magnesium had also resulted in a
22 temporary remission of the clinical signs of BSE."
23 MR PURDEY: Yes.
24 MR WALKER: I have that letter at the moment.
25 MR PURDEY: Yes, it is the first page of one letter that
1 I faxed to Brian McHenry just a
couple of nights ago,
2 where he says that magnesium can either cause an
3 ephemeral remission of symptoms or an acute worsening of
4 symptoms in cows that are suffering from the early
5 stages of BSE. Those are the exact words from memory.
6 MR WALKER: Did he have any explanation for that?
7 MR PURDEY: No, he did not elaborate at all. I was
8 obviously interested that this was squaring up with some
9 of my observations and my colleague farmers.
10 MR WALKER: Thank you. I was going to go on in the article
11 to the following page, page 56. After a section
12 entitled "Enabling Toxins to Bio-accumulate", you then
13 turn on to the question of BSE negative cows. You say
14 that you had read reports of cases where cattle were
15 being slaughtered with BSE symptoms, but proving BSE
16 negative on post-mortem.
17 Then you say that when you read those reports you
18 contacted one of the farmers concerned, who informed you
19 that all three of his herds had been regularly treated
20 with OPs, but it was the two herds farmed on the clay
21 soils that were producing the BSE cases. What was the
22 significance of that, to your mind?
23 MR PURDEY: At that time -- I would disagree with it
24 today -- I thought, because chalk soils are
25 notoriously -- they contain a lot of calcium and
1 magnesium; and my natural
assumption was that the cows
2 grazing over the chalk, being farmed over chalk, would
3 have a much higher status of calcium and magnesium, a
4 correct status. The homeostasis of calcium is
5 controlled by the parathyroid gland, so you can never
6 exactly have too much unless there is a disorder in the
7 parathyroid gland.
8 But whereas I postulated that perhaps this farmer
9 was having problems on the clay farm with magnesium.
10 Indeed, he did confirm that he had to treat, with
11 magnesium, on the clay farm, whereas on the chalk farm
12 he did not get a problem. But you would probably expect
13 that anyway. But it is not quite as simple as that.
14 There are a lot of other sorts of complications with
15 levels of potash and so on which can set magnesium and
16 calcium out of balance, for instance.
17 MR WALKER: Then I was going to go to the last paragraph,
18 but one which begins at the foot of page 56, where you
19 say that:
20 "Standard MAFF questionnaires to farmers with BSE
21 cows only included questions on chemical exposure in the
22 early stages of investigation into the disease.
23 Moreover, MAFF were only concerned with a link between
24 BSE and 'acute' chemical exposure, rather than with the
25 well-known 'delayed' toxic effects of organophosphate
1 poisoning. Yet John Wilesmith,
2 epidemiologist, claimed in a letter to me that my
3 concerns and hypotheses have been covered by the
4 Ministry's extensive detailed research into BSE."
5 The reference that you give for saying that MAFF
6 were concerned with a link only concerned with a link
7 between BSE and acute chemical exposure, I am not quite
8 sure what it is.
9 MR PURDEY: It was the article to which you referred to
10 earlier, one of the original epidemiological trials
11 where it talked about establishing any such association
12 between the immediate effect of a novel chemical used on
13 farms at the time when -- I think they looked at 83 or
14 168 herds from memory.
15 MR WALKER: You are referring to the article in the
16 Veterinary Record in 1988?
17 MR PURDEY: That is right, yes.
18 MR WALKER: Finally you concluded the article by commenting
20 "... a link between BSE and organophosphate
21 treatments is more than plausible, yet MAFF refused to
22 carry out the necessary research to prove or disprove
23 the OP theory."
24 MR PURDEY: Yes, publicly, yes.
25 MR WALKER: Thank you. Now I think that I have covered with
1 you most of the points that you
dealt with in paragraph
2 9 of your statement, which is where you deal with this
3 Ecologist article. I was going to take you to the
4 Western Gazette report, unless there is anything else
5 you want to say about the article itself, no?
6 Then the Western Gazette report is in our year
7 book 1992, if that could be provided please. You will
8 need some help with that other bundle to put it away.
9 I hope that you will find it behind tab 3. Our
10 reference is YB 92/3.19/1.1. I think, in fact, it is
11 halfway between divider 3 and divider 4. Have you found
12 it there? This is a report in the Western Gazette, 19th
13 March 1992. There is reference made to your theory and
14 to the Ecologist article. In the fourth column, we have
15 a comment from Professor Lacey. I quote:
16 "Leeds University professor of Microbiology,
17 Richard Lacey said 'it looks increasingly likely there
18 may be one or more precipitating agents that trigger off
19 BSE and it is possible that insecticides are involved.
20 More study is urgently needed. There is something
21 desperately amiss with the Ministry's approach to the
23 That is the close of the quote there from
24 Professor Lacey. There is then a description in this
25 article of the cases of BSE deaths following the ban,
1 and the discrepancy between the
predictions of the
2 Southwood Report on the number of cases of BSE and the
3 latest figures from the National Farmers' Union. There
4 then follows a further quote from Professor Lacey:
5 "The number of young animals dying should have
6 begun to fall not rise. This strongly suggests the
7 offal ban has not stopped the spread of the disease."
8 At this stage, at any rate, you seemed to have
9 had Professor Lacey on your side?
10 MR PURDEY: Yes. I mean, he was quite an ardent supporter
11 in the early days; and he refereed two of my articles
12 which both recommended publication. In fact, his was
13 the most positive peer review of all the peer reviewees.
14 MR WALKER: Are you referring to The Ecologist article?
15 MR PURDEY: The Ecologist and the Journal of Nutritional
16 Medicine, yes.
17 MR WALKER: We will come on to the Journal of Nutritional
18 Medicine in a moment. If we can just note what
19 Professor Lacey had to say then, I think we move on in
20 this bundle to the letter from the Minister to Mr King.
21 We find that at YB 92/6.8/2.1. This is a letter of 6th
22 June to Mr King. It is about halfway through before you
23 reach divider 7. I think you need to go on a bit.
24 6.8/2.1. That looks like it. Now, this is a letter
25 sent to the Rt. Hon. Tom King, who I think was your MP?
1 MR PURDEY: Yes.
2 MR WALKER: And had passed on some of your concerns to the
4 MR PURDEY: Yes.
5 MR WALKER: And there is some discussion about
6 organophosphates and motor neurones. They are
7 considering the contents of your article, they say.
8 They then turn to genetic susceptibility but say they
9 cannot draw any conclusions on the information currently
11 So that the stance that is taken by the Ministry
12 at this stage is simply one of "we cannot say very
13 much". Would that be roughly right?
14 MR PURDEY: Yes. I mean, at this stage I did experience,
15 perhaps, a slight loosening of the reins. I did feel a
16 slight gap in the clouds appearing, a bit of light
17 appearing, when Gillian Shephard was Minister of
19 MR WALKER: This was actually written by John Gummer,
20 I think, this letter.
21 MR PURDEY: Well, yes, this would just be prior to that.
22 Sorry, I have got the wrong -- yes, that is okay. That
23 would be just prior to the loosening-up period.
24 MR WALKER: Now, also just a period on the chronology here.
25 We are in early to mid 1992. I think we might mention
1 Mustard again. If I take you back
to your article in
2 the Journal of Nutritional Medicine at page 69, you say
4 "In January 1992, due to a shortage of milk quota,
5 the whole dairy herd was moved on to another farm
6 (chemically managed) which had spare quota available to
7 accommodate them. When the herd returned to the organic
8 farm in mid-March 1992, two cows, Mustard and another
9 cow called Damson (who also originated from the same
10 chemically run farm)," this was the same farm that
11 Churnside Birthday had come from too, "were both
12 manifesting the early stage symptoms of BSE.
13 "One 400 ml bottle of magnesium was subcutaneously
14 injected into each cow at the beginning of April. Both
15 cows remitted within 48 hours of treatment."
16 MR PURDEY: Yes.
17 MR WALKER: So they both got better?
18 MR PURDEY: Yes. Normally, with magnesium sulphate, if it
19 was an acute magnesium problem, the cow would invariably
20 remit in one hour to two hours. What was odd about cows
21 -- in fact I would now guess that BSE was the problem
22 if a cow took 48 hours to respond to the magnesium
23 treatment. I know a lot of other farmers who found this
24 48-hour response -- when initially they would think the
25 disease was a magnesium disease, he would inject and
1 have to wait for 48 hours for
recovery. Whereas, if it
2 was a pure magnesium disorder, you would get recovery
3 within an hour ordinarily. This was interesting.
4 MR WALKER: Then in the article, you say:
5 "Damson started to relapse, albeit only
6 moderately, within 1 month of that treatment."
7 MR PURDEY: Yes.
8 MR WALKER: That brings you on to paragraph 10 of your
9 statement, where you deal with Chillaton Damson. You
10 tell us that you refused to hand her over even though
11 she showed signs of BSE, because you wanted to continue
12 to treat her to test your theory about the OP
14 MR PURDEY: Yes.
15 MR WALKER: And you wrote to Mr Meldrum, and he replied on
16 14th July 1992. In our 1992 year book, which you have
17 open in front of you, if you could turn on up to tab 7?
18 I think we will find this at our reference YB
19 92/7.14/2.1. This is a letter you received from
20 Mr Meldrum.
21 MR PURDEY: Yes.
22 MR WALKER: The Chief Veterinary Officer. In paragraph 1,
23 he points out that:
24 "Notification is in our own interest as, if the
25 suspect cattle were to die before there had been
1 inspection, you might lose out on
2 Then he goes on to say that he appreciated that
3 your prime concern is to have the opportunity to carry
4 out further investigations. He says:
5 "I have no hesitation in agreeing to your carrying
6 out further tests on your animal while it is under
7 restriction, with the proviso that it is subject to
8 regular clinical inspection by a veterinary officer.
9 The overriding concern is for the welfare of the animal,
10 and if at any time it is deemed to be suffering
11 unnecessarily, it will be slaughtered."
12 Then he went in the next paragraph to the question
13 of examinations on CNS tissue. He said that with regard
14 to carrying out such examinations after slaughter, he
15 must ask for further information before agreeing to vary
16 their procedures. He made reference to their concerns
17 about the way in which it was investigated. So he asked
18 you for some information.
19 Now, the letter ended by saying that he could
20 assure you that the Ministry had not closed their eyes
21 to the needs of individual farmers, or to the fact that
22 symptoms characteristic of BSE may be caused by other
23 syndromes. He went on to say that treatment with
24 magnesium sulphate had been known to produce complete
25 recovery of some suspects which were clearly affected by
1 hypomagnasemia, not BSE. He
concluded by saying:
2 "None of their investigations linked either
3 clinical signs or development of lesions of BSE with
4 prior treatment with organophosphorous drugs."
5 Then I think that you then deal with subsequent
6 events in the part of paragraph 10 that carries over the
8 SIR NICHOLAS PHILLIPS: Just before we go on, can you help
9 me with this? You are here talking about concluding
10 that the symptoms of this illness was attributable to
11 delayed effects of low dose OP damage.
12 MR PURDEY: (Nods)
13 SIR NICHOLAS PHILLIPS: That again was something that you
14 had referred to in paragraph 9.
15 MR PURDEY: Yes.
16 SIR NICHOLAS PHILLIPS: But when you were looking at making
17 the point that no cow born and raised on an organic farm
18 had died of BSE, you then commented:
19 "The great majority of organic farms had avoided
20 using the high dose type OP."
21 MR PURDEY: Yes.
22 SIR NICHOLAS PHILLIPS: I infer from that that some of them
23 would have been using the low dose type of OP. That
24 raises the question why were they not getting these
25 symptoms if you think it was a low dose effect?
1 MR PURDEY: Basically, it was well
known within farming
2 circles that you could actually sign the form that you
3 treated your cows and never actually carry out the
4 treatment, and an awful lot of farmers have phoned me
5 who did this, who have said that, you know, they are the
6 only farmer in their road who has not had problems with
7 BSE, even though they all fed the same brand of
8 feedstuff. There were actually very few cases where
9 organic farms fell within the compulsory zone. I was
10 one of them, and there was somebody else in Wales who
11 also fell, and they managed to wriggle out of having
12 their cows treated without going to court. I went to
13 court and quashed the order at that time. But I did
14 know one organic farmer who used the Fenthion brand,
15 that is the active ingredient Fenthion, which was used
16 at the 5 milligrammes per kilogramme body weight, as
17 opposed to the 20 milligrammes per kilogramme body
18 weight phosmet chemical.
19 SIR NICHOLAS PHILLIPS: Thank you.
20 MR WALKER: I think you said just now you went to court and
21 quashed the order. In fact, from what you have told us
22 earlier, it was not quashed. What happened was that an
23 agreement was reached between you and the Ministry which
24 meant that you did not have to do what they had said
25 previously you would have to do?
1 MR PURDEY: Yes, but in the High
Court case, I demonstrated
2 that the Ministry were acting illegally by enforcing
3 treatment with a chemical dressing. We argued that
4 under the Animal Diseases Act the Ministry were only
5 empowered to treat with a vaccine or serum. And we
6 argued that an organophosphorus compound was neither a
7 vaccine or a serum. Therefore, the Ministry order was
9 MR WALKER: That was your argument, and the Ministry took it
10 sufficiently seriously at least to reach an agreement
11 with you, but the court did not actually pronounce a
12 judgment quashing the order?
13 MR PURDEY: Well, subsequent to 1985, the Act was amended
14 very rapidly to add "chemical dressing" after "vaccine
15 or serum".
16 MR WALKER: The point was dealt with by legislation, but so
17 far as the legal record is concerned, the order had not
18 in fact been set aside by a court?
19 MR PURDEY: No, I suppose I was the only farmer that had
20 recognised this problem, yes, in the wording.
21 MR WALKER: Thank you. Now, we then have the description of
22 what happened in relation to Damson. I was not going to
23 go into the detail of that. We have all had a chance to
24 read the story of what happened to Damson, but I was
25 going to take you to Mr Bradley's letter of 5th
1 November, which I think comes
towards the end of that
2 story. We have that in the same bundle just after tab
3 11, if you could turn on to it. Our reference is YB
4 92/11.05/1.1. This refers to a letter of 29th September
5 1992, which I do not think that we have found. What
6 Mr Bradley goes on to say about that is that:
7 "We [I think that means the Central Veterinary
8 Laboratory] wish to follow up and clarify some of your
10 Then, in the next paragraph, Mr Bradley goes on to
12 "That Damson had BSE confirmed is beyond
13 dispute... If you are satisfied and agree the final
14 diagnosis of BSE, so be it. However, if you are
15 suggesting that the cow had concurrent chronic
16 OP-induced spongiform encephalopathy, we would like to
17 see the supporting evidence for this conclusion with the
18 agreement of your veterinary surgeon. This would
19 include a clear description of the clinical signs with
20 dates of examination, the nature, result, and
21 interpretation of the blood tests, and when the blood
22 samples were collected in relation to the clinical signs
23 and treatments. We would also like to have the detail
24 of the frequency and method of administration and dose
25 of the drugs used. Although I may be able to obtain
1 some data from colleagues in the
2 Service, it would be convenient if you could also
3 indicate the origin and date of acquisition of Damson,
4 and the treatments with dates, doses, drugs and routes
5 of administration with particular reference to OP
7 Was this something you went on to take up and give
8 all these details?
9 MR PURDEY: Yes, I think I sent the majority of the details
10 to Ray Bradley after that, yes.
11 MR WALKER: And then there are some other aspects of your
12 letter that he raises, asking for documents in relation
13 to the references that you have given. Then, in the
14 paragraph which straddles the page, he says that you had
15 suggested that MAFF should initiate some research.
16 At present, he said, you had presented no new
17 information which suggests this is necessary. But
18 should you be able to present convincing evidence that
19 there is a deficit, your suggestion could be
21 "However, it would be helpful to us in considering
22 any proposals for further research to have a clear
23 statement of the objective or the hypothesis to test."
24 What was your reaction to this response to your
1 MR PURDEY: Well, I felt sort of
that it was putting the
2 onus on me to do the research, which -- obviously I am a
3 very small farmer and I have not got much money, so to
4 do the sort of extent of tests that would be necessary
5 to provide some sound scientific evidence that would in
6 my mind spearhead MAFF to take it up was obviously out
7 of my pocket. All I was able to do was to do what I had
8 been trying to do, to test BSE cows on my farm in
9 relation to the healthy cows on my farm. I felt I was
10 in a no-win situation. I was limited in what I could
11 actually do to achieve that requirement that Ray Bradley
12 was putting on me.
13 MR WALKER: Now, before we leave the 1992 bundle, I just
14 wanted to take you to the letter that we have behind tab
15 12. This is a letter of 22nd December 1992, sent to you
16 by Satoshi Ishikawa, who is the Professor and Chairman
17 of the Department of Ophthalmology at the School of
18 Medicine, Kitasato University in Japan.
19 Did you remember this letter?
20 MR PURDEY: Yes, very much so.
21 MR WALKER: In this letter Professor Satoshi Ishikawa says
23 "Your description of mad cows and warble fly to
24 organophosphates compounds is exactly true."
25 That must have been encouraging.
1 MR PURDEY: Yes, it was. It was a
good New Year's present
2 actually. It arrived on January 1st, from memory.
3 MR WALKER: Do you know how Professor Ishikawa had become to
4 be interested by all that?
5 MR PURDEY: Professor Ishikawa is a sort of long-standing
6 global author on low dose chronic organophosphate
7 poisoning. He was involved in identifying this whole
8 region in Japan, the Seikou(?) district, where he
9 identified a sort of chronic neurotoxic syndrome,
10 particularly amongst children in that area. He had been
11 using the treatments that I was trying to use on my cows
12 on humans with great success, where he was actually
13 curing people with a range of neurodegenerative diseases
14 after a six-month course of treatment. In a sense, he
15 was one of my gurus at this particular stage of my
17 MR WALKER: Is there anything more you would like to say
18 about that letter before we leave 1992?
19 MR PURDEY: I think what was interesting is he was citing
20 vacuolation in the particular neuronal tracts and the
21 nuclei, like the red nucleus, the vestibula, the
22 reticular formation, which correlate precisely with the
23 regions that Wells et al identified as the regions that
24 were vacuolated in their first Veterinary Record paper
25 back when BSE first arose. So Ishikawa seemed to have
1 raised this correlation in a
pathological sense, but as
2 far as the exact detail of the pathology, I am obviously
3 not certain, because it is, you know, couched rather
4 sort of vaguely. I wanted to investigate this a lot
6 MR WALKER: Thank you. That brings me on to 1993. So we
7 can put away this 1992 year book, and you can take out
8 1993. I would like to begin with your letter to Farming
9 News. YB 93/3.26/1.1. It is first document after
10 divider 3. Here we have a letter published in Farming
11 News on 26th March 1993, headed "False Link Made in BSE
12 Case". Is this a letter you sent?
13 MR PURDEY: Yes.
14 MR WALKER: You begin by saying you were enraged to read in
15 many national newspapers last week that links were being
16 suggested between the farmer who contracted CJD disease
17 and his consumption of milk from his BSE-suffering cow.
18 MR PURDEY: Yes.
19 MR WALKER: Then you go on to refer to chemically induced
20 CJD. What was it that enraged you about reading this in
21 the national newspapers?
22 MR PURDEY: Well, I knew that there were no prion protein
23 cell lines expressed in the memory system. Therefore,
24 if prion protein is indeed the infectious commodity, in
25 whatever form, then I could not see, unless of course
1 the udder was damaged by some
mechanical damage and
2 caused an inflammation -- and it is known that prion
3 protein is involved in the lymphatic system, and
4 therefore any inflammation might have prion proteins
5 present; but if a cow has got mastitis, then its milk is
6 not sold. I could not really see the scientific logic
7 in what they were saying.
8 In particular, I was aware that kuru mothers who
9 had breast-fed their children, there was no association
10 between kuru developing in the children of kuru mothers
11 who breast-fed their children, who had themselves
12 developed kuru at a later stage. Kuru is another prion
13 disease, similar to new variant CJD, BSE.
14 MR WALKER: Then, later on in this letter, you said that
15 your trials with your own BSE cow, Damson:
16 "Were spearheading research into chronic OP
17 pesticide induced BSE. It has been proved that some of
18 the OPs that effect the bovine food chain also exhibit
19 serotonin agony, cholinesterase depression and
20 mutagenicity", what you described as, "the dirty three
21 detonators for BSE".
22 Is there anything more that you would like to say
23 about this letter?
24 MR PURDEY: Yes, I mean I still hold to some of that.
25 I remember when I met the Ministry in 1994, James Hope
1 pointed out to me that they had
found no mutagenic
2 association in any cell line with BSE. That is not to
3 say that there is not one, but you know, I hold quite
4 high regard for James Hope, and in a sense I thought
5 that maybe it was not a mutagenic mechanism that was
6 involved, it was something post-translational, that is
7 after the protein has been synthesised in the genetic
8 material, that it was some covalent modification,
9 perhaps after the protein had been synthesised that
10 changed the shape of the protein.
11 SIR NICHOLAS PHILLIPS: Mr Purdey, I noticed in some of
12 your earlier letters or articles that you had yourself
13 been referring to BSE as a "slow viral infection". It
14 sounds as though by this time you had been converted to
15 the prion theory?
16 MR PURDEY: Yes, the further I went on, and I started
17 reading Stanley Prusiner's work. And I think, even
18 though I do not hold to some of the aspects of Stanley
19 Prusiner's and his associates' work, I think that it
20 seems that the prion protein must have some pathogenic
21 ability that is unusual in relation to other proteins
22 that are known to be deformed in the disease.
23 MR WALKER: The next stage in the chronology, I think, is
24 Brainstorm, who was a cow whose mother Churnside
25 Birthday we have been talking a bit about, because in
1 paragraph 11 of your statement,
you tell us that in
2 April 1993 it seemed that Brainstorm was exhibiting
3 symptoms of BSE?
4 MR PURDEY: Yes.
5 MR WALKER: You started treating with magnesium sulphate in
6 the hope of remitting the symptoms?
7 MR PURDEY: Yes.
8 MR WALKER: And on 10th May, the Government vet revisited
9 the farm and took the view that Brainstorm no longer
10 exhibited symptoms of BSE, and withdrew movement
11 restrictions that had been placed on the cow?
12 MR PURDEY: Yes.
13 MR WALKER: Just for the record, I think we have the letter
14 from the Ministry confirming that just behind divider 5
15 in this bundle. If you turn on to that? It is the
16 second document after divider 5. We see here a letter
17 of 11th May, YB 93/5.11/1.1. Is this a letter that you
19 MR PURDEY: Yes.
20 MR WALKER: After the first paragraph which describes what I
21 have just recounted, the second paragraph says that:
22 "Mrs Crea reported that although exhibiting no BSE
23 symptoms, the cow did not appear to be totally healthy."
24 There was then a suggestion that you should have
25 her examined by your own vet. Is there any significance
1 to that?
2 MR PURDEY: I think the first two visits, they obviously
3 thought there was a possibility of BSE because of the
4 symptoms that we observed. It was on the third visit
5 that the symptoms that were suggested of BSE had
6 remitted. And this is why they are saying that -- yes,
7 I mean I would agree with her prognosis at that time,
8 that, you know, it did not look as though the cow had
9 BSE, although I was still aware of -- I was unhappy
10 about the cow. I still thought, you know, that I could
11 still see signs of it. But they were very subtle. She
12 also inspected the cow in the field. When you get them
13 in the building and they have got BSE, the symptoms are
14 exacerbated and the stress of being in the building
15 brings out the symptoms, but on the third visit we
16 examined the cow in the field, and I think, you know,
17 those signs just were not present.
18 MR WALKER: Now, at about this time too, there was further
19 correspondence between you and the Minister or rather
20 your MP and the Minister. If we could look at that? We
21 need to go back to April, so back in the bundle to
22 divider 4. The first document after divider 4 is YB
23 93/4.16/1.1. This is a letter from Mr Gummer to your
24 MP, Tom King.
25 Mr Gummer begins in his letter, which is dated
1 16th April 1993, by thanking Mr
King for a letter of 5th
2 April, which had enclosed letters from you and from
3 Professor Ishikawa. Is that the letter we had seen of
4 December of the previous year?
5 MR PURDEY: Yes, it was.
6 MR WALKER: Then he goes on to say that the hypothesis of
7 spread of disease by infective feed had been
8 substantiated by epidemiological studies. In the next
9 paragraph, he says:
10 "Although there are superficial similarities in
11 histopathology, there are important differences as
12 between BSE and organophosphate toxicity ...", which he
13 says have been agreed and extensively studied and
14 documented by neuropathologists.
15 He then turns to a point about CJD, and says that
16 the Department of Health would be interested to see case
17 reports and medical literature on that.
18 Finally, he concludes by saying:
19 I would add that much research is underway to
20 investigate the many aspects of this group of diseases,
21 including studies on the mechanisms which lead to the
22 development of disease. I enclose a copy of the interim
23 report on research of the Spongiform Encephalopathy
24 Advisory Committee which describes this, and which
25 Mr Purdey may be interested to see."
1 Can I ask you what your reaction
was when you
2 learnt of this letter?
3 MR PURDEY: Well, when I read the list of research that was
4 being carried out, I could not see anything at all that
5 was relevant to my hypothesis, nothing at all. It
6 seemed to be all tailored to investigate the official
7 scrapie leap theory as the cause, and some work on the
8 prion protein, but that obviously involved -- you know,
9 they were saying that the abnormal prion from sheep had
10 jumped into cows and mutated, or whatever it was.
11 MR WALKER: Now, I think you have mentioned in your
12 statement that you wrote again to Mr King and that
13 letter was forwarded on to the new Minister of
14 Agriculture, Mrs Shephard. We see her reply just after
15 divider 6. Our reference is YB 93/6.16/1.1. This is a
16 letter dated 16th June 1993, from Gillian Shephard to
17 Tom King, referring to a letter that Mr King had sent
18 Mr Gummer on 17th May. In the second paragraph,
19 Mrs Shephard said this:
20 "Although OPs can react with a variety of
21 biological substances, I am advised that OP poisoning
22 differs so greatly from BSE that the link is most
23 unlikely. Clinically, OP poisoning is so dissimilar to
24 BSE that the two are unlikely to be confused, and there
25 is no evidence to link any immunotoxic or mutagenic
1 effects of OPs with BSE. The
papers provided by
2 Mr Purdey have no bearing hypothesis. Two of them are
3 concerned with conditions in man which have some
4 features clinically similar to CJD, but not
5 pathologically. I would add that research on BSE is the
6 responsibility of our Central Veterinary Laboratory,
7 where there is also considerable expertise in OP
8 toxicity in farm livestock."
9 That is the end of the quote. Again, what was
10 your reaction to receiving a copy of that letter?
11 MR PURDEY: Well, firstly I do not agree that -- she had
12 not differentiated between acute OP poisoning and
13 chronic OP poisoning, which show markedly different
14 symptoms and pathology. It was a mainstay of my theory
15 that this was a chronic problem, if you like, a high
16 dose chronic problem. And this had been sort of
17 ignored. This vague generalisation was in a sense a
18 misrepresentation of what I was actually saying.
19 Also, I can never recall having linked the
20 immunotoxic effects of acute high doses of
21 organophosphates to BSEs because work has shown that in
22 mice the immune system is actually required for the
23 disease process to ensue, because when they have
24 engineered mice with an immune knock-out, they cannot
25 develop the disease.
1 So, I think what is relevant is
the fact that
2 organophosphates will actually accelerate some aspects
3 of the immune and cytokine system, which could have
4 great relevance to the BSE disease process, I believe.
5 This was really a misrepresentation of what I was going
6 trying to say. But I agree I had linked the mutagenic
7 effects of OPs to the disorder; but my work has evolved,
8 and I no longer really feel that mutagenicity has a role
9 in the disease.
10 PROFESSOR FERGUSON-SMITH: Still, at that time you still
11 felt that the disease was caused by a combination of an
12 environmental factor and the prion, is that not right?
13 MR PURDEY: Yes.
14 PROFESSOR FERGUSON-SMITH: It seems that this particular
15 letter does not recognise that.
16 MR PURDEY: Yes, that is right.
17 MR WALKER: There seems to have been some movement in
18 Government thinking about what they should do about
19 organophosphates shortly after this, because we have in
20 our Purdey references bundle -- if I could ask you to
21 keep hold of the bundle you have at the moment, but also
22 to be given the Purdey references bundle, and turn to
23 tab 10 -- we have, at tab 10, an article from the Sunday
24 Telegraph dated 22nd August 1993. It is by Greg Neale,
25 the Environment Correspondent for the Sunday Telegraph.
1 If you can be shown the document?
You see it begins:
2 "The Government is reviewing the safety of
3 chemical veterinary products, including some used in the
4 home, amid fears that they could be linked to illness in
5 farmers using sheep dip, or even bovine spongiform
6 encephalopathy - BSE or 'mad cow' disease.
7 "Gillian Shephard, the Agriculture Minister, has
8 ordered the review of all veterinary products containing
9 chemical organophosphates, including flea collars used
10 on cats and dogs as well as on cattle and sheep ...
11 "An Agriculture Ministry spokesman said yesterday
12 that the review did not mean there were grounds for
13 linking 'mad cow' disease with OPs as has been suggested
14 by some researchers."
15 Then, later in the article, reference is made to
16 what is said by a spokesman at the Animal Health
17 Division, which is consistent with what I have just
18 quoted. Then Ian Gardiner, the head of the NFU, on farm
19 policy, is quoted as saying:
20 "So far, nothing has happened that increases the
21 probability that the Ministry's hypothesis of what
22 caused BSE is wrong. Government advisers have advised
23 the minister and the NFU has no basis on which to differ
24 from that advice."
25 Then the article goes on. Sir Richard Body, the
1 MP for Holland with Boston and
former chairman of the
2 Select Committee on Agriculture Pesticides, said:
3 "We have not got on top of BSE, and there is a
4 grave suspicion that there are other reasons for it. The
5 Ministry made up its mind too quickly."
6 What did you know about the proposed review at the
8 MR PURDEY: Well, I did not know anything about it at all.
9 Certainly in relation to BSE, I was not aware that there
10 was any proposed review into looking at the chemicals as
11 a possible link to BSE or CJD.
12 MR WALKER: I would like to take you, I think, to the piece
13 that appeared in the Western Morning News at about that
14 time, unless there is anything more about what you would
15 like to say about what we see from the Sunday Telegraph
17 MR PURDEY: No.
18 MR WALKER: That means, I think, that we can put away this
19 bundle. We come back to the bundle that you have open.
20 If you turn to tab 8, our reference is YB 93/8.20/1.1.
21 This is an article in the Western Morning News which is
22 headed "Pesticide May Lead to Mad Cow Disease". I think
23 here that you say that -- or rather are quoted as saying
24 that -- you believe evidence was growing that the OP
25 chemicals could be linked to the disease, and that
1 Government scientists believe mad
cow disease was
2 triggered by contaminated cattle feed, but critics claim
3 that OP chemicals may have been to blame.
4 There is then a quote from the MAFF spokesman
5 saying that it is quite clear that feed is the main
6 source of the infection, although mother to calf
7 transmission could not be ruled out. Then reference is
8 made to the review that is proposed by Gillian Shephard,
9 and a quote from you, if I can take the second
11 "The Ministry's epidemiologist, John Wilesmith,
12 tells me that their extensive investigations have
13 covered my theory, but they admit not having done
14 detailed studies of delayed effects of cumulative low
15 dose OP toxicity."
16 MR PURDEY: Yes.
17 MR WALKER: When had Mr Wilesmith told you that?
18 MR PURDEY: I was referring to -- when I said "they", I was
19 referring to the Ministry in general. I had heard a
20 taped interview with a member of, I think, the
21 Veterinary Products Committee or the Veterinary
22 Medicines Directorate, who stated that when he was asked
23 whether he had looked at the chronic low dose effects,
24 he said "No, they had not".
25 MR WALKER: Unless there is anything more that you want to
1 say about that article, I would
like to move on to --
2 MRS BRIDGEMAN: Could I just ask one question? It so
3 happens later in this article that somebody suggests
4 that the Department of Health ought to be involved.
5 I wonder whether throughout this story, up to this
6 stage, you had had any direct dealings with the
7 Department of Health rather than the Ministry of
9 MR PURDEY: No, I had not, no.
10 MRS BRIDGEMAN: Was this because it did not occur to you,
11 or for some other reason?
12 MR PURDEY: I suppose because I was a farmer, I was
13 immediately involved with the agriculture. I think BSE
14 was always considered a farming issue, an agricultural
15 issue. But they did come in at a much later date.
16 SIR NICHOLAS PHILLIPS: Could I just ask about this
17 article? It reports MAFF making the point that there
18 was clear evidence linking BSE to feed. At this stage,
19 was that something that you would have regarded as
20 simply incompatible with the theories that you were
21 putting forward, or something that could accommodate
22 these theories?
23 MR PURDEY: Well, there were a few slight, sort of, weak
24 points of my theory which I was trying to grapple with
25 at the time, which, you know, the Ministry have pointed
1 out. One was the Channel Islands,
which was never a
2 compulsory warble fly eradication zone. Having said
3 that, exactly the same systemic types of phosmet were
4 used on the island for control of lice. Because it is a
5 very warm winter climate on the islands, that is
6 conducive for lice to breed.
7 I still did not feel particularly happy with that
8 line of attack on my theory. I did not feel that
9 I addressed it. I thought maybe, you know, that
10 feedingstuffs had a role in taking in the
11 organophosphates that are bioconcentrated -- such as the
12 systemic phosmet -- that are bioconcentrated in the fat
13 of the meat and bonemeal, and fat was a large account of
14 the cattle feed rations on the Channel Islands because
15 they were producing Channel Island milk, which was very
16 high fat milk.
17 I am a Channel Island cattle breeder myself, and
18 it is common policy to use even protected fat, and
19 rations up to 20 per cent of animal fat in the
20 concentrate feed. I think perhaps this could explain
21 why you have this particularly high incidence of BSE,
22 particularly on Guernsey Island. I was also stressing
23 that maybe the genetics of the Guernsey cow, what would
24 have been close inbreeding of the Guernsey cow on the
25 Channel Islands, and of the Jersey on Jersey Island, and
1 this may have lead to low levels
2 enzymes in the livers of Guernsey Cows. Perhaps -- and
3 this is total hypothesis, but I was requesting at the
4 time that that should be looked at at the meeting I had
5 with the Ministry in due course.
6 SIR NICHOLAS PHILLIPS: Thank you.
7 MR WALKER: Could I just ask you a bit about the Department
8 of Health? We saw in that letter of 16th April 1993
9 from Mr Gummer that he said that the Department of
10 Health would be interested to see your references.
11 I noticed that when Gillian Shephard wrote, she said
12 that the references that you had provided were concerned
13 with conditions in man which have some features
14 clinically similar to CJD, but not pathologically?
15 MR PURDEY: Yes, I think maybe they had overlooked the
16 spongiform. But I suppose they could have been arguing
17 that this particular type of pathology in BSE, which is,
18 as I was describing earlier, this intensive
19 glycosylation was not similar to the type of spongiform
20 encephalopathy in the couple of articles that I produced
21 as references. It could have been a very fine point,
22 but I do not know.
23 MR WALKER: All I was seeking to draw from this was that at
24 least in April of 1993, MAFF were saying to you that the
25 Department of Health would be interested in some
1 references. It seems from the
letter of June 1993 that
2 you indeed sent the references on to MAFF?
3 MR PURDEY: Yes, I did, yes.
4 MR WALKER: So they could no doubt pass them on to the
5 Department of Health. But that the only comment that
6 you were getting back about the references that you had
7 sent in was that they had no bearing on your hypothesis,
8 as far as I can see from this correspondence?
9 MR PURDEY: Well, I sent in a considerable number of
10 references. I can remember, I think, about 40 published
11 peer-reviewed articles that dealt with -- because no one
12 had put this together, I was just substantiating facets
13 of the whole BSE disease issue with this particular
14 specific article from the published peer-reviewed
15 literature by way of assimilating my case. That was,
16 after all, the only means of my disposal, because I did
17 not have a laboratory and I had to rely on other
18 published peer-review evidence from experimental work,
19 et cetera.
20 MR WALKER: Thank you. Now, the next thing I would like to
21 take you to is an article by Dr Richard North, which is
22 the next page in that bundle. Our reference is YB
24 This is an article headed "The corruption of
25 Science", which appeared in something called UKEPRA News
1 on 20th August 1993. Do you know
what UKEPRA stands
3 MR PURDEY: I think it is better to ask Richard North.
4 Maybe someone present understands.
5 MR WALKER: In this article, Richard North describes some of
6 the work you had been doing, and he also described,
7 I think, what had happened in relation to Damson, is
8 that right?
9 MR PURDEY: Yes, I think so, yes. I was not actually aware
10 of this exact article. I was aware of an article that
11 Richard North had written in The Times. I think that
12 this was virtually the same article by the looks of it.
13 MR WALKER: I have taken you to it because it is referred to
14 in a letter that you have told us about in paragraph 10
15 of your statement, the letter of 21st October. If you
16 turn on to tab 10, it is just before the end of tab 10,
17 just ahead of tab 11. Our reference is YB
18 93/10.21/1.1. This is a letter that Mr Wilesmith of CVL
19 sent to Mr North, who begins by saying:
20 "Dear Mr North, I have been asked to write to you
21 about your article 'The Corruption of Science' in UKEPRA
22 News of 20th August, to draw attention to a number of
23 facts that seem germane to the issues you have raised."
24 In this third paragraph, he refers to the causes
25 that were tested against the then known facts. In the
1 second to last sentence, he says:
2 "At those meetings a number of experiments were
3 reported which clearly show that material from brains of
4 animals showing clinical signs of BSE can pass on an
5 infectious neurodegenerative disease to some other
6 species of animals. It is difficult to see how evidence
7 of this kind could support a theory that BSE is simply
8 due to chronic OP poisoning."
9 Was your theory that it was simply due to chronic
10 OP poisoning?
11 MR PURDEY: Yes, I mean it could have been as a result of
12 some knock-on effect of organophosphate. For instance,
13 in my Journal of Nutrition and Medicine article,
14 I hypothesise that the organophosphate somehow, by
15 malforming the prion protein, would then evoke an
16 autoimmune attack on the extra large sort of molecular
17 conglomeration of the prion fibril at the end of the
18 disease process. This could set off a type of
19 autoimmune attack that did not display the normal
20 inflammation that one would expect in the pathology of
21 an autoimmune disease, merely because prion protein
22 seems to have a role in activating lymphocytes, et
24 So when the prion protein is damaged, you would
25 not have the normal inflammatory attack. So by