Now that Professor John Walker-Smith has been cleared of charges brought against him by Britain’s General Medical Council – with an admonition by the appeals judge that such a travesty must never happen again – his testimony can be called something important:
When he was just a witness trying to defend himself, up against an aggressive prosecution, Walker-Smith testified for many days about how he treated the 12 children who came to make up the Lancet medical journal case series, published in 1998. In great detail, he explained how the children were referred to him; what he and his colleagues discovered, and what they decided to do about it.
Constantly urged to speak up and slow down, Walker-Smith, now in his 70s and long-retired, was vigorous in his defense of his treatment of the children and the accuracy of the Lancet paper he co-authored.
His testimony – now affirmed by the appeals judge as those of an honest and experienced practitioner whose medical license has been restored – demolishes many of the myths perpetrated about the Lancet paper. Those myths, promulgated first by Brian Deer at the Murdoch Sunday Times of London, and then by the British Medical Journal and its editor, Dr. Fiona Godlee, elevated co-author Dr. Andrew Wakefield to an all-powerful manipulator of the children’s case histories.
Wakefield falsely claimed the children were consecutively referred, so the myth went; he turned unremarkable childhood bowel problems (“diarrhea,” in Deer’s sneering dismissal) into some sort of scary new disease; he claimed the children were autistic when most had no such diagnosis; he ordered invasive medical procedures solely to serve his own research needs; and he finessed the timing of the MMR shot to suggest it might have triggered the symptoms, in one case even putting the shot before the symptoms, not after where it belonged. (It’s important to remember that Walker-Smith was the treating physician, Wakefield the researcher who was collecting data.)
As the BMJ said in its own press release about its January 2010 allegations: “In an editorial, Dr Godlee, together with deputy BMJ editor Jane Smith, and leading paediatrician and associate BMJ editor Harvey Marcovitch, conclude that there is ‘no doubt’ that it was Wakefield who perpetrated this fraud. They say: ‘A great deal of thought and effort must have gone into drafting the paper to achieve the results he wanted: the discrepancies all led in one direction; misreporting was gross.’” (Earlier this year, Wakefield sued the BMJ, Godlee and Deer for defamation. Our series “An Elaborate Fraud” is addressing the fraud allegations.)
What follows is a very small sampling of Walker-Smith’s own words, words that speak eloquently in his own defense and, inevitably, to the veracity of such claims about the paper and its other key author, Andrew Wakefield.
Q. “Professor, I want to ask you again about a phrase which you have used in your evidence in dealing with correspondence, and the phrase is, “clinical need”. What do you mean when you use the term, “clinical need”?
A. Well that is basically that a child has got a problem and we need to find an answer to why the child has a problem, and that means that there is a need to indicate investigations in a child. If a child has got significant gastrointestinal symptoms, a pattern suggesting a particular disease, we then try and find out what is wrong with the child. A child who is diagnosed with something and some problem is continuing, the clinical need is to find the appropriate treatment for that.
Q. In relation to the 12 children in the Lancet paper, … on what basis did your department investigate these children?
A. We investigated them exactly on that basis of clinical need. These children had symptoms and signs. We did not know what they were due to. We undertook a series of investigations to find out what was the problem with the child and there were outcomes from these investigations and they came in the traditional way. We made a diagnosis and eventually, where it was appropriate we gave treatment. …
What is quite astonishing about this review of children is the high evidence of abnormality. In suspected Crohn's disease [another GI disease]… we had a lower incidence of abnormality. Here we have mucosal abnormality in 47 of 50 children investigated with the autistic spectrum [the first 12 comprised the Lancet series], which almost suggests that this could be a feature of autism per se, although these are children all with bowel problems.
The children were all investigated specifically and exclusively by clinical means to determine whether bowel inflammation was present that could then be appropriately treated. …
Q. From your evidence, and indeed it is borne out by the documentation, that the early cases that you saw of the children who became the patients reported in The Lancet, you started with the premise that they might have classical IBD [inflammatory bowel disease], that they might have Crohn’s disease or ulcerative colitis?
A. Indeed, we did. … My whole focus and I believe my colleagues’, was first, “Did these children have Crohn’s disease”. Things change, as we have heard, as time went on.
Q. As time went on, and you were not encountering Crohn’s disease, what did you understand to be the condition or the problem that you were encountering? If it was not Crohn’s disease or ulcerative colitis, what did you believe that you were finding?
A. Just like many times in my career before, we were finding a new disorder. … We were beginning to see a new syndrome, fairly clear features of children presenting with diarrhoea, very often abdominal pain which often was not diagnosed by other doctors. Sometimes [that] was because of the children not speaking and the fact that screaming and other manifestations were not obvious. [Those] were the chief symptoms. Then, as we found, constipation or, more appropriately in some ways, faecal loading or certainly something interfering with gut transit was a feature as well. There is a characteristic symptom pattern.
Then, rather more remarkably in a way, there was a remarkable homogeneity in the histopathology [microscopic examinations]. It is a subtle pathology, the cardinal features being particularly ileal lymphoid nodular hyperplasia [swollen lymph nodes], very often colonic lymphoid nodular hyperplasia, and a general increase in inflammatory cells in the lamina propria, and there was evidence of acute events with cryptitis and abscess formation from time to time. It was an entity not so different from an adult practice called microscopic colitis, but clearly in the context of autism we felt something new was coming, and that is the motivation, of course, for us clinicians to feel that it was appropriate for Andy Wakefield to take the lead, and write these features for publication.
Q. Having gone through the histology reports, the synthesis of those reports in the histology meetings, it is clear that there are abnormalities there ---?
Q. --- which you identify as abnormalities and explain why?
Q. But they are not particularly florid?
Q. They are not, as you accept, either Crohn’s or ulcerative colitis?
A. That is true.
Q. But can one say, really they are not terribly serious? They do not really matter very much because they are not more florid than what has been described in the histology reports?
A. No. They clearly matter. I can say they really matter because of the subsequent work led by Simon Murch. Ralph Furlano’s memorable paper published, I think, in the Journal of Paediatrics, which established significant immuno-pathology of a great[er] severity than is apparent with the light microscope. …
In fact, I think Simon Murch had called this “a subtle enteropathy”. We did have to educate Sue Davies at the Royal Free in the interpretation of small bowel biopsies as well [her reports finding no problems was the basis for Deer’s claim that Wakefield altered the pathology reports to falsely show bowel disease]. On that occasion, Alan Phillips played a major part, because he was an expert on the small intestinal morphology. So it was not a surprise to me in any way that these were new findings, new findings emerging, as we saw a group of children we had not studied before.
Q. Is the size – perhaps that is the wrong word. Is the extent of the inflammation found proportional to the symptoms that the child suffers? In other words, is there a relationship, that if you get big lesions, if you happen to have cryptitis, crypt abscesses, it is going to be more painful and more uncomfortable than something more minor?
A. No, no. There is never that simplistic agreement between pathology and clinical findings. But furthermore, what are you doing with biopsies? It is like taking a post stamp out of a tennis court, and the endoscopist is taking little pieces of tissue, and giving them to a histologist to look down the microscope. The great importance of endoscopy is that you can see the whole of the colon, for example, and we saw in one circumstance, when Simon Murch saw a number of lymphoid follicles in the colon but by chance none of them were present on histology. That was because, by chance, he had not biopsied from an area where there were these findings. So we cannot expect a simplistic correlation between little pieces of tissue and the global picture. The more biopsies you take, of course the better chance there will be.
Q. What about the suggestion that in fact all you are seeing is a normal variant of the gut pathology that children would have in any event? So this is not really indicative of inflammation at all, that this, particularly lymphoid nodular hyperplasia is simply a variant of normal, with no clinical significance. I stress clinical significance.
A. I rely in terms of pathology on Professor Paul Dhillon, a very distinguished histopathologist, co-author of the Lancet paper. I had nothing whatever to do or knowledge of the histology that he and his team did but his opinion is that there is significant histopathology there. My role as a clinician is the taking account of those significant, in his judgment, histopathological findings. I regard them as serious and worthy of treatment.
The difficult area in relation to lymphoid nodular hyperplasia relates to the ileum, not the colon. In Professor Dhillon’s view, in my view, it is clearly an abnormal finding, even though the mucosa is otherwise histologically normal. On the issue of the severity of ileal lymphoid nodular hyperplasia, I have to bow to my endoscopy colleagues, because I relied upon them. When the diagnosis of lymphoid nodular hyperplasia was made, I relied on the judgment of Simon Murch and Mike Thomson, apart from those cases in which I relied on the radiologist when the lymphoid nodular hyperplasia was diagnosed on barium study.
[On consecutive referral:]
A. The only way to attempt to find out or refute the charge in relation to consecutively referred was to look at the endoscopy and biopsy book in the department and just see what the facts were in relationship to whether they truly were in the 12 first autistic children who I had considered needed ileo-colonoscopy and actually had ileo-colonoscopy. As well as that we looked at the notes of all the children – rather I did not so much as Mike Thompson did. I was feeling in a bit of a state of shock at that time with this threatening of being reported to the GMC [by Brian Deer, even before the first Sunday Times article had run], but he helped me and we looked through the notes …
Q. The allegation relates to the method of referral. Did you look at the documentation?
A. We looked at the method and in fact Dr Thompson did that for me. He looked up the particular parts and we went through it child by child. I must say the vice-Dean was walking around all the time and supervising what was going on, and was asking us questions about how we were getting on and what was involved. So Professor Humphrey Hodgson was deeply involved in the whole process as well.
Q. By that stage you had retired, and so were no longer in the department?
A. I had completely retired and this came suddenly out of the blue. With no notice I had to go into the laboratory and the best way to try and refute this charge was to look at the consecutive children who had been endoscoped and biopsied out. I went through that book, and I noted each child who had autism and bowel problems and I was able to confirm within that period that the first twelve children were the twelve children in The Lancet paper.
Q Can we just look at what you wrote. … “A statement by Professor John Walker-Smith: I deny the allegation that there was systematic bias in the pattern of referral for the children in the 1998 Lancet paper. No children were invited to participate in this study. Upon review of the Centre for Paediatric Gastroenterology, Royal Free Hospital, work book entitled ‘Biopsies Vi 4/9/95 to 21/7/97’, we confirm that the children who were reported in The Lancet paper of 1998 were the first 12 children consecutively referred to the university department of paediatric gastroenterology with autism and related disorders, who had gastrointestinal symptoms requiring ileo-colonoscopy to exclude chronic bowel inflammation.” …
[Quoting from another letter by Walker-Smith] “In relation to this department, we are all in agreement with the description of a new syndrome of ileal lymphoid nodular hyperplasia and non-specific colitis in a cohort of self-selected (ie parent selected) patients. We have sent a paper to the Lancet and I enclose a copy for you. In some there is a clear historic link to MMR.
“In another paper Andy is preparing, he is describing the evidence for measles virus. This is far, far stronger than for Crohn’s disease in histochemical studies etc. I believe in this small number of patients who may be at risk in any event of autoimmune disease, measles may have played a role. [This paper was not published.]
“Like you I am very concerned at any weakening of MMR uptake in the community. However, I have personally seen all these ‘autistic’ children and in some at least there seems to be a strong presumptive evidence of an MMR link.”
Q … Did you have concerns at the time about the potential or possible role of MMR in the pathogenesis of the conditions described?
A. Yes. There is a real risk and concern about measles viruses from the second paper. As I think Professor Candy told this Committee, he had seen the second paper which contained Andy Wakefield’s immunopathological data concerning the persistence of measles virus in tissues from some of these children. I think that knowledge was at the back of one’s mind when allowing this matter to be discussed at all because if there obviously was a possible role, and I would say an impossible role, for measles virus in pathogenesis in the light of those immunohistochemical findings.
Q. So this would be based upon the scientific findings outside your personal experience?
Q. Rather than the rather rough and ready epidemiological evidence from the parents?
A. Absolutely. This was not just recall of the parents; this was objective evidence and Dr Wakefield had presented that data as a poster at the British Society of Gastroenterology in Harrogate that year, so it had been looked at by the British gastroenterology community and had caused some interest. The data was not sufficient to say that he proved, by any means, that measles virus was present in the tissues of these children, but there was an interesting observation that he had made suggesting that the measles virus was there. …
Q. [Referring to a document dated 8 October 1997:] It is what has been described as the final version of the first Lancet paper is being circulated?
Q. Once this circulation in October had occurred, Professor Murch recalls that you proposed there should be a review of the histology slides for The Lancet 12, particularly by all the pathologists who were co-authors, so that they could satisfy themselves that the description of the pathology in the draft paper was correct?
A. I do not remember that.
Q. Do you recall that the pathologists who were co-authors were in agreement with the wording or description of the histology that appeared in The Lancet?
Q. And how do you recall that happening? Just before you answer that, let me make it clear that it is Professor Murch’s recollection that that consensus was reached because a meeting, as the one I have just described, took place. How do you recall this consensus arose?
A. It is possible, but I recollect at some point bumping into Paul Dhillon and had an informal exchange. I do not remember any of these particular events, I am afraid. But I have no doubt that what Professor Dhillon had in the paper was accurate and correct.
Dan Olmsted is Editor of AgeOfAutism.com and co-author, with Mark Blaxill, of “The Age of Autism – Mercury, Medicine, and a Man-made Epidemic,” published in paperback last year by Thomas Dunne Books.