An Elaborate Fraud, Part 4: News Analysis -- The British Medical Association Is “Standing Up for Doctors” Even If It Means Attacking Patients
Dream On

Time To Revisit Deer Part 3

Brian deer By Martin Hewitt

This is the third part of an analysis of Brian Deer’s (in photo) claims that Dr Andrew Wakefield fixed the findings in the 1998 Lancet paper 'Ileal-lymphoid-nodular hyperplasia' (Lancet, 1998; vol. 351, p.637), a small clinical case series of 12 patients with autism and bowel disease treated at the Royal Free Hospital in 1996/97. The British Medical Journal editors not only published Deer’s claims on 5 January 2011 [HERE], but backed them with the charge of academic fraud against Wakefield. Using the UK General Medical Council (GMC) transcripts and research papers, Parts 1 and 2 questioned the way Deer selected his evidence to support serious allegations of fraud.

Scientific fraud

To substantiate scientific fraud the accuser must show that the original findings were changed – ‘fixed’, ‘falsified’, ‘fabricated’ in the BMJ’s words – to advance a particular interest or theory that the original findings do not support. These analyses of Deer’s claims test if this is so. Part one examined Deer’s claim that three of the nine children reported with regressive autism did not have an autism diagnosis [HERE]. Part two examined the claim that, despite the paper claiming that all 12 children were ‘previously normal,’ five had documented pre-existing developmental concerns” and could not have regressive autism [HERE]. Deer used GP records and local consultants’ letters from the early 1990s that were not available to Wakefield and his team when investigating the Lancet paper children in the mid-1990s, and which only became available 16 or so years later to the GMC fitness to practice hearing against Dr Wakefield and Professors John Walker Smith and Simon Murch sitting between 2007 and 2010. Of the volumes of documents used as evidence in the GMC hearing, the Royal Free team in the mid-1990s would have only the following: the General Practitioner’s (GP) referral letters summarising each child’s case; four consultants’ letters which two GPs appended to their referral letters; and the results of their own clinical investigations at the Royal Free. The two analyses of Deer’s evidence showed that he selected extracts from the GMC transcripts that appeared to support his claims but failed to examine statements from the GMC hearing that countered his claims. That medical clinicians disagree over the interpretation of symptoms – as the GMC hearing showed in abundance – does not constitute fraud. In other words the first two analyses of Deer’s evidence found no evidence of Wakefield’s alleged fraud.

Deer’s claim

The third and present part examines Deer’s claim that “In nine cases, unremarkable colonic histopathology results—noting no or minimal fluctuations in inflammatory cell populations—were changed after a medical school ‘research review’ to ‘non-specific colitis’”.  Seen in the context of an article claiming Wakefield fixed his results, this claim suggests further fixing took place by colleagues, not just Wakefield, attending the review. However, as discussed below, the review was a means whereby clinicians reached agreement on the different interpretations of the children’s bowel condition. This claim is examined in the light of the published GMC transcripts of the hearing against the three doctors. Child 11’s case is the exception – a private patient from the US, his case was discussed only in passing and so cannot be independently verified from the GMC transcripts. So nine cases becomes eight. We can judge the accuracy, selectivity and interpretive license Deer applies to his evidence against Wakefield. His claims that Wakefield fixed his results are summarised in a list of bullet-points at the end of his BMJ article.

Deer’s article provides little in evidence to back up his third claim. Of the nine children, only child 3 is singled out as “a prime example” of a bowel disease case. No evidence is provided in the body of the article on the other children’s bowel condition. We examine what Deer says about this child before commenting on the other seven children. The procedure is simple: Deer’s quotes and his endnotes referencing GMC and other evidence are given in italics followed by other statements of evidence from the GMC ignored by Deer. We end up with two lists of statements from the GMC: one from Deer supporting his allegations and the other from GMC witness statements countering his claims – both lists containing matching statements that contradict each other. Of course disputation is the stuff of scientific debate and the driver of scientific progress. But at no point can disputed statements count as evidence of fraud. They cannot stand as the last word on whether Wakefield fixed his results when other statements by medical clinicians and experts to the GMC hearing undermine the thrust of his allegations of fraud – a charge the GMC did not level against Wakefield or the other two doctors.

The children

This is what Deer says of child 3.

Quote 1 “What was unquestionably true was that child 3 had serious bowel trouble: intractable, lifelong, constipation. This was the most consistent feature among the 12 children’s symptoms and signs but, being the opposite of an expected finding in inflammatory bowel disease,  it was nowhere mentioned in the paper.

108 a) Ajjegowda Shantha. GP records and evidence to the panel. Day 5. (b) John Walker-Smith. Evidence to the panel. Day 91.

109 Murch S, Thomson M, Walker-Smith J. Author’s reply [letter]. Lancet 1998; 351:908

110 Squires RH and Colletti RB, Indications for pediatric gastrointestinal endoscopy: A medical position statement of the North American Society for Pediatric Gastroenterology and Nutrition. Journal of Pediatric Gastroenterology and Nutrition 1996; 23: 107-110.

111 Ian Booth. Evidence to the panel. Day 41. “Looking for inflammatory bowel disease would be a most unusual way of approaching a patient with severe, long-standing constipation.”

 

Deer’s central contention is that, although the children, including child 3, may have displayed bowel symptoms, none had inflammatory bowel disease (IBD) as claimed in the Lancet paper, and that at worst they had constipation which Deer claims was not consistent with IBD. However the lack of mention of constipation in the Lancet paper is evidence of its initial and provisional status as a small case series – which the Lancet called an ‘Early Report’ – which presents initial findings that subsequent more rigorous research sustains or refutes. As the research developed after 1998, further papers by Royal Free team members referred to constipation in the context of IBD, supporting contradictory findings that challenge what Deer says about the children’s bowel ‘trouble’:

  • Furlano RI et al. 'Colonic CD8 and γδ T-cell infiltration with epithelial damage in children with autism', Jn Pediatrics 2001, 138, 3.
  • Torrenti, F et al. 'Focal-enhanced gastritis in regressive autism', Am Jn Gastroenterology 2004, 99, 598-605.
  • Afzal N, et al. 'Constipation with acquired megarectum in children with autism', Pediatrics 2003, 112:939-42.

Regarding endnote 110, the protocol was issued in 1996, prior to the above research, and considers the use of endoscopy in general paediatric gastroenterology. It does not address the use of endoscopy in diagnosing gastroenterological problems in autistic children.

Regarding 111, the above research into the presence of constipation in the context of IBD suggests a different view to Professor Booth's. Further, the following exchange took place at the GMC hearing between Walker-Smith’s counsel and Dr V Miller, defence expert witness in gastroenterology: "Q  Staying with constipation, do you come across constipation as a feature of inflammatory bowel disease? A  Absolutely, yes” (Day 101-38).

So the 1998 paper was the first of several papers on autism and bowel disease from members of the Royal Free team which subsequently went on to develop more rigorous findings, including the co-presence of constipation and IBD and the significance of the children’s histopathology.

Deer goes on to argue that, following the initial histology reports, the bowel findings were changed by a medical school “review” – a statement suggesting that, if the changes amounted to ‘fixing the data’, the responsibility lay with participating colleagues seeking agreement on conflicting histopathology readings. Responsibility for these changes cannot rest on Wakefield alone, contrary to what the BMJ editors’ contend in their accompanying editorial to Deer's piece.

Quote 2: as I revealed in the BMJ last April, the hospital’s pathology service found the children’s colons to be largely normal, but a medical school “review” changed the results.

115  Deer B. Wakefield’s “autistic enterocolitis” under the microscope. BMJ 2010; 340:838-41.

What Deer’s article does not reveal are the purpose, rigour and exemplary professionalism of these reviews that “changed results”. Without more exact procedures to determine medical findings associated with autism and bowel disease, early findings must inevitably rely on individual interpretations, with their greater risk of error and inexactness. Yet these same moves towards accuracy, when subject to critical peer review among scientists and clinicians, play an important role in reaching greater accuracy in interpretation. In the case of histological readings of bowel samples, different histopathologists can arrive at different readings. Given the critical importance of these findings for the outcome of the patient’s clinical care, a process of checking and debating different views is imperative. With this in mind Professor Walker Smith instituted two new practices to review the biopsies of children treated by his team, including, but not limited to, the Lancet 12: first, weekly clinical reviews of the histological findings attended by general histopathologists who had produced the initial reports, an expert in bowel histopathology, the appropriate clinicians and medical scientists; secondly, a blinded review of the initial histology findings conducted by the expert bowel histopathologist (the GMC panel did not examine the blinded reviews). The transcripts record the added rigour the weekly reviews imposed, in subjecting initial reports, constrained by time and resources as witnesses indicated (see eg Day 33-3), to close scrutiny and a deliberative process of reaching consensus on their significance. Work pressures on the hospital pathology department meant that the Lancet children were one small group among 700 or so cases per week received from different departments (Day 3 – 36).

Apart from child 3, Deer provides no evidence in the body of his article to support the claim that “unremarkable colonic histopathology results” were changed for the other eight children. The nine children can only be identified from the table attached to the article, where under a column headed ‘non-specific colitis’ he compares what was said in the Lancet paper for each of the 12 children with what he claims the records show, placing a ‘Yes’ or ‘No’  against each child to substantiate or refute the Lancet data. 'No’s' are placed against child 3, 4, 5, 7, 8, 9, 10, 11 and 12. Whereas the Lancet said that these children exhibited findings of non-specific IBD, Deer claims these children showed “unremarkable” histopathology results that were subsequently changed.

Given the significance of this claim for his general claim that Wakefield fixed the Lancet paper results, it is surprising that this evidence is not included in the article itself (apart from child 3’s). Deer confines the evidence to a different paper which readers of his BMJ article may have missed. A link ‘web extra’, to a ‘background document’ with Deer’s data, is found on the left column of the article’s webpage. This goes to a pdf document – each page headed with Deer’s own web address – on a separate part of the BMJ’s website. The ‘web extra’ provides two tables separating out the content from the single table in the article into Table 1, what the Lancet paper says, and Table 2, what Deer says. In Table 2, the column refuting the existence of non-specific colitis has ‘no’s’ and a footnote against each of the nine children. The footnotes cite the first histology reports on the children’s biopsies (small and large bowel biopsies numbered I, II, III, etc) produced by the Royal Free’s general histopathologists, other reports and Deer’s comments. No reference is given to the findings of the later blinded readings by the expert bowel histopathologist and scant reference to the more rigorous analyses of Walker-Smith’s weekly reviews. Important parts of the Royal Free team’s research procedures and findings are missing.

If the initial histology reports written by the Royal Free’s team of general histopathologists, which Deer quotes in his footnotes to Table 2, are compared with the subsequent data from the expert histopathologist in gastroenterology available to the GMC, we see markedly different readings regarding the presence and extent of inflammation in the children’s bowel. We will look in detail at the matching reports for child 3 first and then, to save time, compare short extracts from the matching reports for the other seven children (excluding 11). Bold text is used throughout to emphasise conflicting statements in the matching reports.

CHILD 3

Quote 3: [Footnote] 56. Histology report. ‘I. Shows small bowel mucosa with an increase in intra-epithelial small lymphocytes, but no architectural abnormality. II. Shows small bowel mucosa with prominent lymphoid follicles. III-VII. Each show large bowel-type mucosa within normal histological limits.’ The pathology service comments: ‘Mild inflammatory and reactive changes in the small bowel samples, of uncertain significance on morphological grounds alone. No microbes or granulomas identified in any of these samples.’”

The initial histology report for child 3 – in common with initial reports for the other 8 children – identifies signs of inflammation which are considered unproblematic. By contrast child 3’s discharge summary written by Dr David Casson (a member of the Royal Free team and co-author of the Lancet paper) on 16 September 1996 draws on the further histopathology review of the results and stresses the pathology of inflammation in the child’s bowel:

“Overall appearances were normal until the ascending colon. Here one definite apthoid ulcer was seen and towards the caecum there were multiple prominent colonic lymphoid follicles. The terminal ileum also appeared abnormal showing marked lymphonodular hyperplasia though there was no ulceration. Histology possibly demonstrates mild chronic inflammation within the lamina propria of the terminal ileum. It should be noted that it is difficult to estimate whether or not this is within normal limits. … Throughout the large bowel there was a patchy increase in chronic inflammatory cells with an occasional prominent lymphoid follicle with a germinal centre. There was also an occasional focus of acute cryptitis within the ascending colon. There was also mild crypt distortion. …. The patchy distribution of this inflammation and the involvement of the terminal ileum are in keeping with a diagnosis of Crohn’s disease.

Subsequently the diagnosis of Crohn’s was replaced by ‘non-specific’ or ‘indeterminate colitis’, reflecting the limited knowledge in the paediatric gastroenterology community in the mid-1990s of how to read bowel symptoms in autistic children. Professor Walker-Smith explains his logic at the time: “I believed these children had significant inflammatory bowel disease but it was not Crohn’s disease and was not ulcerative colitis. That is why the actual words, ‘indeterminate colitis’ were used here” (Day 74-42-3).

CHILD 4

Quote 4: 60. Histology report. “I. Small bowel type mucosa with a lymphoid follicle. II-VII. Large bowel mucosa, some with attached muscularis mucosae, with no evidence of architectural distortion or increase in inflammatory cells in the lamina propria. Lymphoid follicles with germinal centres are present in many of the biopsies. No cryptitis or crypt abscesses are seen. The surface epithelium appears intact. No granulomas, ova or parasites are seen.” The pathology service comments: “Large bowel series with terminal ileum, with no histopathological abnormality.”

Comparing this initial report with the following exchange between Walker Smith and his QC, we see why he took the subsequent results more seriously and why he placed more credence on the reports of the expert bowel histopathologist, Dr Dhillon:

Q Just take as an example – we could do the exercise and I am going to do it in due course when we go through the individual cases, but in some cases Dr Dhillon appears to have found a description of the pathology there that is not present in the original report.

A There are differences. There are some children where there are differences, yes.

Q Taking as an example ... Child 4...You have written there....

A It says, “Lymphoid nodular hyperplasia. Dhillon differs – 2/5 Paneth cell metaplasia. Increased eosinophils 5/5 mild increase in inflammatory cells”, And then I have written after that, “routine – normal”, rather as an aide memoir to myself saying that the routine report had been reported as normal....

Q ....I asked you whether the Dhillon findings were the same as the routine, were they in all cases the same as the routine?

A ....They were not the same in all cases, no.

Q Taking that as an example, you have got “Dhillon differs” – you have written that to yourself.

A I have.

Q What did you mean by that?

A  He considered that there was more significant histopathological abnormality than the routine report. Obviously the routine report says it is normal and he, for example, says, “Mild increase in inflammatory cells”. I agreed with that, otherwise I would not have written it.

Q And 2/5, what does that mean?

A That is the two out of five paneth cells there was metaplasia

CHILD 5

Quote 5: 64 Histology report. “Specimen I consists of fragments of small intestinal mucosa which includes lymphoid follicles but which is without pathological abnormality. Specimens II, III and IV are large bowel mucosa fragments with normal crypt architecture. There is at best a minimal increase in chronic inflammatory cells within the superficial lamina propria. No active inflammation is seen. Specimens III and IV show minor crypt architecture distortion, including occasional bifid forms. Paneth cell metaplasia is not seen. No excess chronic inflammatory cells are seen. A very occasional polymorph is seen within surface crypt epithelium. No ova, granulomas or parasites are seen in any of these biopsies.” The pathology service comments: “Large bowel series; minor changes the significance of which are uncertain but do not amount to the diagnosis of inflammatory bowel disease.” Also of interest: child 5 was reported by endoscopist and Lancet co-author Simon Murch as not having ileal lymphoid hyperplasia, but the published Lancet paper said that he did have this.

Child 5’s discharge summary which the Royal Free sent to the GP is referred to on Day 11 (p.52): “he has apparently been having bouts of diarrhoea on and off since he was 4 years of age. There is no blood or mucous in the stool. He has occasional abdominal pain during which he suddenly clutches his abdomen and flexes his knees. This has a duration of about 10 minutes and then resolves.

The histology report in footnote 64 is discussed in Mr Miller's examination of Professor Walker-Smith (Day 78-45/6), which again provides insight into how he read  the histology report in a way significantly different from Deer.

Q I would like your comments on the findings first.

A Specimen I is in accord with the endoscopic appearances. The II, III and IV, “there is minimal increase in chronic inflammatory cells within the superficial lamina propria”, that is a definite abnormality that suggests chronic inflammation, but the adjective “minimal” is used and there is “no active”, that means acute, inflammation. III and IV says “minor crypt architecture distortion including occasional bifid forms”. That clearly indicates that there has been previous damage from inflammation, damage in crypt architecture, and the crypts have responded to that abnormality by, instead of having a single form, they have developed a double or bifid form.

In III and IV the opinion was that there was no excess chronic inflammatory cells and a very occasional polymorph was seen within the surface crypt epithelium. That is certainly abnormal, which is an indicator of some acute inflammation.

CHILD 7

Quote 6: 72 Histology report. “I-II. Two pieces of small intestinal type mucosa with essentially normal villous architecture. There is no increase in inflammatory cells in the lamina propria or in intraepithelial lymphocytes. Part of a lymphoid follicle is included. No parasites or granulomas are identified. III-IV. Sections from all sites show large bowel mucosa with no abnormality of crypt architecture or significant increase in inflammatory cells in the lamina propria. Some of the biopsies contain lymphoid follicles. No granulomas or parasites are seen.” The pathology service comments: “Small bowel biopsy and large bowel series without significant histological abnormality.”

The colonoscopy report showed “Slight evidence of vascular abnormality in rectum and sigmoid but otherwise essentially normal.  The terminal ileum however demonstrated a marked degree of lymphonodular hyperplasia” (Day 1 – 57). Commenting on his post-admission letter to Child 7’s GP, when examined by GMC QC Ms Smith, Walker-Smith points out: “It was an interesting letter from my perspective because clearly something had been found that was considered significant”, namely the finding of evidence of bowel inflammation and indeterminate colitis” (Day 6 – 31). Again Walker-Smith, drawing on his long-standing experience and expertise in gastroenterology, placed greater significance on the presence of lymphonodular hyperplasia.

CHILD 8

Quote 7: 76 Histology report. “I. These are both fragments of poorly orientated, but normal small bowel mucosa. A lymphoid reactive centre is seen in each sample. II-IV. These are all pieces of normal colonic type mucosa containing occasional lymphoid aggregates. Minimal inflammatory changes may be the result of operative artefact.”

Following GP treatment for constipation, child 8 was admitted to her local hospital after she became unsettled during the night, was screaming for a week, had diarrhoea (“6 bowel motions/day) and complained of abdominal pain. On arriving at the Royal Free, the question for Professor Walker-Smith was whether the histology report indicated the presence of inflammation in the bowel. In his examination by Ms Smith, he rejects the general histopathologist’s suggestion that signs of inflammation were artificial due to problems in extracting the biopsy (an ‘operative artefact’), rather than evidence of real inflammation, because there was insuficient time for the small bowel specimens to become inflamed after removal (Day 80 – 37). Walker-Smith concludes that it is “Not Crohn’s or ulcerative colitis, no, but the fact reported there is “minimal inflammatory changes”.

When Mr Miller QC questions Dr Miller, the defence expert witness in gastroenterology (Day 103-6), about the presence of inflammation in child 8’s bowel, he replies, “No, it is not entirely normal. It is not, frankly, grossly abnormal, but a lymphoid reaction is implying, as we have discussed in previous patients, that there is some overactivity of the lymphoid tissue, thereby implying some degree of inflammation.”

CHILD 9

Quote 8: 80 Histology report. “I. Small bowel mucosa showing no histological abnormality. II-VII. Large bowel mucosa showing prominent lymphoid follicles but no histological abnormality.”

Again at variance with the general histopathologist’s original report above, the colonoscopist’s report found “a marked increase in the size and number of prominent lymphoid nodules”, which Walker-Smith relayed to the GP, adding that, “The colon was endoscopically normal except for an area at the hepatic flexure which was slightly erythematous. Histologically there was an increase in chronic inflammatory cells throughout the colon with a moderate increase in intra-epithelial lymphocytes.... Our diagnosis is indeterminate colitis with lymphoid nodular hyperplasia” (Day 4-13).

Later Dr Miller, when examined by Mr Miller QC, explained that large bowel mucosa showing prominent lymphoid follicles was “...an unusual feature because lymphoid hyperplasia...is normally in the terminal ileum” (Day 103 - 16).

CHILD 10

Quote 9 : 84 Histology report. “I. The specimen consists of small bowel and have sampled a Peyer’s patch. Where present, the overlying villae appear unremarkable. The lymphoid tissue shows reactive changes. Parasites and granulomas are not seen. II-VI. All these biopsies show large bowel mucosa with occasional isolated bifid glands. The inflammatory population is within normal limits. Parasites and granulomas are not seen.” The pathology service comments: “No significant histological abnormality.” A supplementary report was requested, following a weekly histology meeting with clinicians, and possibly with Wakefield. This said: “These biopsies have been reviewed following a clinicopathological meeting. The ileal biopsy shows confluent lymphoid aggregates within otherwise unremarkable small intestine. The large bowel biopsies show a very subtle scattering of chronic inflammatory cells within the lamina propria. The superficial lamina propria contains focal nuclear debris and the surface epithelium appears slightly degenerate. No active inflammation is seen. More levels have been cut and no granulomas have been identified.” The pathology service comments: “Minor abnormalities. ? Significance.” Child 10’s biopsies were also examined at another centre. Following the supply of samples to the University Hospital of Wales, Cardiff, Huw Jenkins, consultant paediatric gastroenterologist, wrote: “I’ve now had a chance to review 10’s intestinal biopsies kindly sent down from the Royal Free hospital, and although there are lymphoid follicles present in the small intestine these are often regarded as a normal finding, and certainly our pathologists here would suggest that the colonic biopsies were within normal limits. Certainly they do not feel he has good evidence of gut inflammation in the biopsies.”

The long footnote records a process of uncovering problematic signs in child 10’s bowel which are not initially understood. First, the general histopathologist’s report identifies reactive changes in the lymphoid tissue, but no significant histological abnormality. Secondly, the biopsies were reviewed, which confirmed the initial findings, but uncertainty remains over their significance. Thirdly, but absent from the footnote, Dr Murch’s colonoscopy report (Day 25 - 59) states unambiguously, “This colonoscopy was definitely abnormal, in probably a more striking example of the pattern seen in the cohort of the autistic children. The rectum showed definite mild abnormality, with a slightly granular mucosa and abnormal vascular pattern. Prominent lymphoid follicles could be seen throughout the colon, with no other mucosal abnormality. The caecum showed an eryhthematous, granular mucosa around a swollen ileo-caecal valve, while the terminal ileum showed minor inflammatory change and striking lymphoid hyperplasia distally. I suspect that the biopsies will show unequivocal abnormality!”

When these concerns were placed side by side with the University Hospital of Wales report, which viewed the biopsies as unproblematic, the Royal Free clinicians had to decide whether child 10’s inflammation was pathological and required treatment. Presumably because of their experience and duty of care, the team decided that treatment was warranted.

CHILD 12

Quote 10: 92 Histology report. “I-IV. Pieces of large bowel mucosa including lymphoid follicles with germinal centres. There is no architectural abnormality and no increase in inflammatory cells in the lamina propria. No organisms or granulomas are seen.”

Again in the hands of an expert gastroenterologist, the unremarkable is viewed with more concern. Dr Murch finds “Appearances almost normal to caecum. Again there were minor changes in the rectum and caecum (slight changes in vascularity and prominent lymphoid follicles). The ileo-caecal valve could not be identified”. Pieces of large bowel mucosa including lymphoid follicles with germinal centres...” (Day 25 - 63). Examined by Mr Miller QC, Professor Walker-Smith summed up his conclusion that “the finding of lymphoid follicles, especially with germinal centres, in the large bowel mucosa is an abnormal finding” (Day 82 - 21).

Conclusion

This study of the GMC transcripts shows that Deer has constructed his allegations of fraud against Wakefield in two ways. First he redefines what constitutes fraud. Academic fraud is no longer confined to researchers who deliberately change their original data in publications promoting scientific preconceptions the original data do not support. According to this conventional view, the accuser would have to compare only the researchers’ own original data with the published data. For Deer fraud is committed and substantiated if there is, besides the original research data, additional data the researchers did not have access to that is different from the published data. We have seen that Deer either did not have access to or did not use all the original data generated by the Royal Free team, such as the results of the blinded histopathology reviews and the weekly reviews. But we have also seen that Deer makes considerable use of additional information, such as GP and local consultant records which the Royal Free team would not be aware of at the time the case series was conducted. For example, the first and second analyses of Deer’s article showed that he drew on GP and local consultant records, most not available to the team, that appeared to show that three of the children were not autistic and that five (including child 11) had pre-existing developmental concerns before and not after the MMR. The analyses used other statements, some from the same witnesses, to show that the children were indeed autistic and that the pre-existing conditions were not relevant to the conditions that did emerge after MMR (except for one child who had the measles jab before his MMR). Of course these different views may be matters for further debate – though relating to records taken in some cases 20 plus years ago. But the fact that debate is possible means these are not matters of indisputable truth, against which differing findings can be viewed as fraudulent.

The second way in which Deer constructs his case for fraud is by selecting statements from the GMC hearing in such a way that differences of interpretation and matters of legitimate scientific debate are foreclosed to produce the impression that the selected statements stand as the only account available. For example, when we compare Deer’s evidence with other statements from the GMC transcripts, we see that there were differences in the conclusions clinicians reached on the significance of the children’s bowel symptoms, specifically regarding the evidence of inflammation. But rather than acknowledge the normal scope of interpretative variation in histopathology findings, Deer provides the reader only with the ‘unremarkable’ accounts of the initial histopathology reports in seeking to undermine the histological evidence of ‘non-specific colitis’ in nine of the 12 children summarised in the Lancet paper.

Deer’s reconstructions of scientific fraud – of the definition and data determining fraud – are endorsed by the BMJ editors in an editorial introducing his article. The editors allege that “Wakefield altered numerous facts about the patients’ medical histories in order to support his claim to have identified a new syndrome”. Yet not one example of an original fact altered to fit a preconceived syndrome – so constituting fraud – is given by Deer or the BMJ. Discrepancies between the Lancet published data and other data refer in the main to data the Lancet team did not see because they were not part of the original findings. Where data were changed, this was part of the routine processes of reviewing data to seek greater factual accuracy and of reaching a consensus on different interpretations. Not only Deer but more surprisingly the BMJ editors represent the routine but complex processes of making clinical judgments as fixing the data - a travesty of the clinical process.

Deer’s binary view of the truth – where this is no room for interpretation, debate over gradations of meaning, and for reaching consensus – obscures the true nature of clinical investigation and the process of medical advance.

 

 

Comments

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Jenny Allan

http://www.naturalnews.com/033130_Protect_IP_Act_websites.html
Your website is under threat -BEWARE!!

Kerbob

How often are we now told the MMR-autism story is over and let's get back to supporting the MMR and the vaccine schedule.
---------------------------------------
Every time the media and the vaccine-manufacturing drug companies exploit the public by fabricating a vaccine sales SCAMDEMIC, stealing very large sums of US tax dollars in the process, they are liable for the blow-back.

The best defense is a strong offense. Starting kicking Wakefield and everybody forgets the US is $7,100,000,000.00 emptier as a result of yet another highly successful drug company scamdemic.

Wonder why they all smirk.

http://kerboblog.blogspot.com/2011/08/bad-samaritans-wild-ride-or-things-we.html

Jenny Allan

http://www.news-medical.net/news/20110801/Widespread-institutional-corruption-in-American-science-scientist-says.aspx

This says it all!!

Jenny Allan

http://www.stephentemple.co.uk/articles/biasing-bbc-coverage-favour-mainstream-science-opinion/

It's frightening the way that public voices and information are currently being systematically suppressed in the UK. The BBC has just commissioned a review by geneticist Professor Steve Jones, (why him?? and why a review anyway??), about future media UK coverage of science, which includes medical issues such as vaccines and important public decisions on GM foods. Prof Jones wants us to be told only what 'mainstream opinion' dictates - a scary outcome designed to eliminate minority or dissenting views.

The recent UK Government Science and Technology report on peer review, (mentioned in Martin Hewitt's comment below), states:-
http://www.publications.parliament.uk/pa/cm201012/cmselect/cmsctech/856/85611.htm
"Post-publication review in an era of new media and social networking tools, such as Twitter, is very powerful. The widespread sharing of links to articles ensures that research, both accurate and potentially misleading, is rapidly spread across the world. Failings in peer review can, rightly, be quickly exposed. However, there is no guarantee that false accusations of failings will not also be spread. Pre-publication peer review still has an important role to play, particularly in relation to assessing whether manuscripts are technically sound prior to publication. However, we encourage the prudent use of online tools for post-publication review and commentary as a means of supplementing pre-publication review. (Paragraph 211)"

In view of what Martin Hewitt and others are saying about the S&T committee's views, which appear to agree with Brian Deer's Wakefield et al's 'fraud' assertions, this report would appear to be expressing concern about Internet public exposure and criticisms of articles such as Deer's.

Apparently there are also UK moves to attempt to control what is posted on the Internet and even remove websites and comments which are claimed to be 'misleading'. In other words, establishment propaganda will be the ONLY information permitted to be published, broadcast or posted on the Internet.


Martin Hewitt

Deer's disclosures and non-disclosures is part of the much broader agenda to rewrite the history of the MMR saga and bring it to a final close. How often are we now told the MMR-autism story is over and let's get back to supporting the MMR and the vaccine schedule.

The innocent view of history is that it is written on the basis of facts alone. But when history is left to journalists and the powerful voices like the Murdoch press, we get only one view of the facts filtered and selected to produced a view of history according to corporate interests that seek to protect the commercial concerns of the pharma. Deer and his advisers from the MedicoLegal Investigations, allied to the Association of the British Pharmaceutical Industry, through the GMC/BMA/BMJ, to the latest report on peer review from the UK Parliamentary Select Committee on Science and Technology all speak with one voice on Wakefield's 'fraud'. Yet few of them have compared Deer's evidence with the evidence available in the GMC hearing. This version of history starts from the selected facts that cover up GMC testimony supporting the ethical and honourable conduct of Wakefield and the other two doctors. But soon each of these institutional centres of power - the media, the medical profession, Parliament - fall in line with this now dominant version of history. So historical truth gets sedimented into the UK's institutional fabric rather like spreading rumours in Chinese whispers. We have a textbook case in how to discredit critical voices.

Of course just to say these things gets us branded as conspiracy theorists. But note especially who are the people branding us and note the power they exercise in the media and other institutions. I have no idea if Deer and the Sunday Times are being resourced by the pharma and I don't have the resources to investigate this question. So it is not important, other than the fact that these powerful interests speak the same talk. What is vitally important is to revisit Deer's version of history, check it out against the available record (the GMC hearing), and bring it to the attention of individuals and institutions interested in the true record.

The unstoppable rise in the numbers of autistic children in the UK, US and elsewhere, and its crippling impact on public services and the economy, not to say on family life, is the one fact that no one can deny and which will eventually produce the necessary research into the causes of autism. The questions Wakefield asked in 1998 will come back to haunt governments, pharma and media.

John Stone

Media Scholar

Not sure what the protocol is on this although it isn't usual to publish these forms and you should expect to see anything significant in the published declaration. Deer does not disclose the support he received from MedicoLegal Investigations (an outfit allied to the Association of the British Pharmaceutical Industry which specialises in getting doctors before the GMC) in 2003-4.

http://www.whale.to/v/mli.html

It also looks as if BMJ (with its annual pharmaceutical award ceremony) is taking a very relaxed view on hospitality. I suspect this goes back to policy decisions made in 2008:

http://tinyurl.com/3oyeqwy

They refused to post eletters from me earlier this year pointing out that Deer was speaker at a pharma/GSK sponsored conference in Baltimore last November (no doubt he was a key-note speaker)

http://briandeer.com/speaker.htm

http://www.actox.org/AnnualMeeting/MeetingSponsors/tabid/5198/Default.aspx

After much argument and a certain amount of circumlocution Deer does disclose his dealings with the GMC in 2004-6, but of course these were not made known at the time when he was reporting the story in the Sunday Times (nor last year in BMJ when I was complaining about it).

http://www.ageofautism.com/2010/05/godlee-must-go-bmj-fails-to-answer-question-on-deers-competing-interests.html

His funding from BMJ is disclosed, but not as a competing interest. Furthermore, while BMJ quietly acknowledged its competing interests regarding their award ceremony

http://www.bmj.com/content/342/bmj.d1335/reply

http://www.bmj.com/content/342/bmj.c7452.full

http://www.bmj.com/content/342/bmj.d1678

their disclosure still doesn't acknowledge BMJ's business partnership with Merck via BMJ Learning and Univadis. And quite outrageously none of this information is available to anyone visiting Deer's articles on-line, although it is plainly relevant information.

Then, of course, there is the issue of Harvey Marcovitch as BMJ editor signing the journal's allegation of fraud against Wakefield, on the basis that he was not doing it in his capacity as head of GMC panels:

http://www.ageofautism.com/2011/01/harvey-marcovitch-and-brian-deers-investigation-the-lord-high-everything-else.html

Not to mention editor Fiona Godlee's long term commitment to suppressing debate on vaccine safety about which she declared her colour just prior to being appointed to her job:

http://www.ageofautism.com/2011/01/fiona-godlee-editor-with-an-agenda.html

It seems to me that BMJ not only fail in the detail they completely fail in the spirit of disclosure.

Angus Files

The company then trawled through other documents, including its cash authorization records, and found 130,000 pounds’ worth of payments to a group of officers over several years, according to officials with knowledge of the inquiry. Included within those records was documentation of a thousand-pound cash withdrawal around the date of Mr. Goodman’s e-mail concerning his purchase of the Green Book from a police officer, according to one person with knowledge of the investigation.

Same article as below

Angus Files

New York Times

"Mr. Goodman said that he did not want to go into detail about cash payments because everyone involved could “go to prison for this,” "

http://www.nytimes.com/2011/07/30/world/europe/30letter.html?_r=4&hp

Mr Deer might be already on his way....

*Media Scholar*

The author has completed the unified competing interest form at www.icmje.org/coi_disclosure.pdf (available on request from him)
--------------------------------
Why is this not available by *them*?

If *they* don't have this information disclosed publicly and *they* expect the *public* (*we*) rely upon *him* it is not publicly disclosed. *He* is, therefore,holding it privately.

How do *we* know what *he* gave *them* is the same thing *he* gave *us*? *We* don't know unless *they* publicly disclose, what *he* gave *them* originally, to *us*.

If *it* didn't occur to *them* that *they* should disclose *their* fatal conflicts of interest to *us* it is most likely *they* also know *he* has some, and doesn't want *us* to know.

The fact *they* don't want *us* to see *his* conflict(s) of interest means *they* don't trust *him*.

Angus Files

Rupert's Worst Nightmare Come True?
Guardian's Nick Davies comes to U.S.


http://www.adweek.com/news/press/ruperts-worst-nightmare-come-true-133799

Remember Deer,Fitzpatrick and Bustin all boasted about the US work
... http://www.jabs.org.uk/pages/yazbak-expert.asp

Benedetta

I just now get it about Brian Deer and the reason for his employment status.

He doesn't really - really work for anyone.
New's media just picks up a story by a independent reporter because of how interesting it all was - can't blame them.

In a small way I feel sorry for Brian Deer. Out there in the lone world, trying to survive doing his dream job, but really no talent for it, so very vunerable to the forces of evil, so opened to temptation by evil. They really had to hunt high and low for such a Patsy

GennyGC


Dr Wakefield interviewed by Jan Irvin on the excellent gnosticmedia.com

http://www.gnosticmedia.com/dr-andrew-wakefield-interview-vaccines-and-rupert-murdochs-callous-disregard-120/

John Stone

This was information which appears at the end of the first of Deer's BMJ articles in January:

'Funding: Brian Deer’s investigation was funded by the Sunday Times of London and the Channel 4 television network. Reports by Deer in the BMJ were commissioned and paid for by the journal. No other funding was received, apart from legal costs paid to Deer by the Medical Protection Society on behalf of Andrew Wakefield.'

'Competing interests: The author has completed the unified competing interest form at www.icmje.org/coi_disclosure.pdf (available on request from him) and declares no support from any organisation for the submitted work; no financial relationships with any organisation that might have an interest in the submitted work in the previous three years; BD’s investigation led to the GMC proceedings referred to in this report, including the charges. He made many submissions of information but was not a party or witness in the case, nor involved in its conduct.'

'Provenance and peer review: Commissioned; externally peer reviewed.'

http://www.bmj.com/content/342/bmj.c5347.full


Media Scholar

Um, does anybody know where Brian Deer's conflict of interest/competing interests declarations are located at British Medical Journal?

I don't see them.

oneVoice

Vaccines,drugs can damage the intestinal mucous membranes.
That is where about 80% of the body's defense system present
(intestinal immune system).So when kids have IBD and painful
cramping and constipation there is a damage done to the bowels,which will result in an increased permeability of
substances(antigens) into the bloodstream.Chronic inflammation will increase the permeability and the intestinal damage/disruption/inflammation/immune system stress will start effecting the other developing organs.
BMJ and Deer are on Pharma payroll,they should be ashamed
of their lies and cover-ups.Somebody also has to pay for the
damage to Dr. Wakefield's lost wages and and the long list of other damages.Deer better save his money,this war is not over yet.

Seonaid

Thank you Martin for an excellent overview and for all the hard work it must have entailed. And it is well timed. There has been a new surge of media attacks on Dr Wakefield recently - more than likely because of the Murdoch hacking scandal. Maybe someone, somewhere is nervous that the public will put two and two together and start questioning the methods, veracity and motives behind Brian Deer's statements? It terrifies me that Brian Deer can come out with known lies and readily have them published by that now-we-know corrupt media. Has there ever been in history such a sustained attack on an individual without anyone challenging the truth of the content? In a flash back to 2002, have a look at the articles which were allowed airing in the UK press.
http://www.jabs.org.uk/pages/mmr/main.asp?month2=6&year2=2002
There is a fair number of news items questioning the safety of MMR. Can you imagine that happening now-a-days? Dark forces indeed at work here - the media in a strangle hold.

Here is a John Rappoport's interview with Dr Wakefield that sets the record straight.
http://www.progressiveradionetwork.com/the-jon-rappoport-show/2011/7/28/the-jon-rappoport-show-072711.html

marcia

Why can't a lawyer go after the papers who are publishing Deer's fraudulaent claims?

Autism Watcher

"Deer’s central contention is that, although the children, including child 3, may have displayed bowel symptoms, none had inflammatory bowel disease (IBD) as claimed in the Lancet paper, and that at worst they had constipation which Deer claims was not consistent with IBD."

Symptoms and stool patterns in patients with ulcerative colitis.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1433596/

Twenty seven per cent of patients with active colitis voided hard stools indicative of constipati­­on, however, and this was more common in active, than quiescent colitis (p less than 0.05). This feature is probably secondary to faecal stasis in the proximal colon, and an apt descriptio­­n of the bowel disturbanc­­e in ulcerative colitis, irrespecti­­ve of the extent of disease is that the colon suffers from proximal constipati­­on and distal irritabili­­ty.

------------------------------

Patients with irritable bowel syndrome or constipati­­on have an increased risk for ischaemic colitis (IC)

http://www.ncbi.nlm.nih.gov/pubmed/17919313

This study found that patients with a diagnosis of IBS or constipati­­on had a two- to threefold greater risk for IC than patients without these diagnoses.

------------------------------------

Syracuse Gastroeter­ologists Associates

http://www.syracusegastro.com/colitis.html

Constipati­on may develop during active flare-ups of ulcerative colitis. In ulcerative colitis, constipati­on may occur when the inflamed rectum triggers a reflex response in the colon that causes it to retain the stool.

-----------------------------------------

Symptoms of irritable bowel syndrome in ulcerative colitis in remission.

http://gut.bmj.com/content/24/3/190.abstract

Contrary to expectatio­ns these symptoms were not confined to patients with distal disease. Other symptoms such as constipati­on were also very common in the colitic group (31%).

-------------------------------------------------

Microscopi­c colitis: a retrospect­ive study of clinical presentati­on in 53 patients.

http://www.ncbi.nlm.nih.gov/pubmed/15761974

To evaluate the relationsh­ip between symptoms and microscopi­c colitis (MC) subtypes: to test whether collagenou­s colitis (CC) and/or lymphocyti­c colitis (LC) might be related to both constipati­on and diarrhea.

RESULTS: Twenty-thr­ee (43.39%) of MC patients had chronic constipati­on . Twenty-fou­r (45.28%) of patients had autoimmune disease

----------------------------------------

Reevaluati­on of Clinical Features of Ischemic Colitis Analysis of 68 Consecutiv­e Cases Diagnosed by Early Colonoscop­y

http://www.ncbi.nlm.nih.gov/pubmed/8888435

Chronic constipati­on and prior history of abdominal surgery were commonly associated in both young and old patients. Early colonoscop­y, especially by the 3rd day from the clinical onset, is essential for the accurate diagnosis of IC

---------------------------------------

Collagenou­s colitis: constipati­on or diarrhoea?

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1773752/

Various case presentati­ons in the literature have reported that frequent watery diarrhoea introduces the clinical picture of collagenou­s colitis and intermitte­nt or continuous diarrhoea can remain. 2 On the other hand, numerous cases never suffer from episodes of watery diarrhoea but suffer from chronic constipati­on.

-------------------------------------

Environmental risk factors in Crohn's disease and ulcerative colitis: an update.

http://www.ncbi.nlm.nih.gov/pubmed/20117338

Rapid increase in Crohn's disease (CD) and ulcerative colitis (UC) incidence in developed countries, occurrence of CD in spouses and lack of complete concordance in monozygotic twins are strong arguments for the role of environmental factors in inflammatory bowel disease (IBD).

-------------------------------------------

Environmental influence in ulcerative colitis starts in early childhood

Sonnenberg

http://jech.bmj.com/content/62/11/992.abstract

Conclusions: The analysis suggests that environmental factors responsible for the temporal and geographic variations of ulcerative colitis start to exert their influence during early childhood.

"In summary the study showed that development of UC is strongly influenced by one or several environmental risk factorsthat act during a short period of life prior to the age of 5 years."

Autism Watcher

"As made clear in the article, the core data on which the findings were based were evidenced, except in the case of one child, by the transcript of a General Medical Council fitness to practise hearing which sat between July 2007 and May 2010."

Fiona Godlee

Does the transcript of oral testimony available from the GMC contain medical records , medical data , bipopsy material , blood samples , pathology slides , MRi film or any other clear data in regards to this issue ?

If not how is it possible to put forward to the general public a clear and unequivocal argument for research fraud without reviewing the evidence in entirety ?

"It is primarily based on Royal Free hospital records, including histories taken by clinicians, and letters and other documents received at the Royal Free from GPs and consultants."

Fiona Godlee

Are those documents the BMJ refer to above part of the GMC transcripts ?

If so .....

What ethical processes were there to ensure patient confidentiality ?

How were these records released to the BMJ for the undertaking of the peer review process and editorial checking ?


Angus Files

In a year or so possibly sooner, Mr Deer could be up to his neck in the phone hacking scandal possibly the computer hacking scandal as well.

What other method could Deer have obtained detail that even the parents weren’t acquainted with..most of his lies were lies, and still are un supported lies.

"Trojan" emails that gives a hacker full access to a target computer's contents by infecting it with a virus."

http://www.guardian.co.uk/uk/2011/jul/29/scotland-yard-computer-hacking-task-force

Well done Martin posted earlier but its lost in cyber somewhere...


Angus

John Stone

Anyone reading this who isn't eaten by bad faith will understand why it is fundamentally impossible for Andrew Wakefield to have commited a fraud in this paper. What is happening of course globally is that the allegations are being made as if they were true by constant repition.

I also recommend this new post on ChildHealthSafety:

http://childhealthsafety.wordpress.com/2011/07/29/british-medical-journal-fraud/

Sandy

After the recent revelations concerning the scandalous and illegal methods being employed by journalists to gain information, the time is now ripe for subjecting Mr. Brian Deer to intense scrutiny.

Debra

Very well written Martin , its really quite sad to think that , with awards and the like that at the end of the day Mr Deer will only ever be famous for trying and i strongly suggest the word trying , of TRYING to bring down the reputation of a very caring doctor Andrew Wakefield , thats ok Andrew while he is talking about you , he is keeping you in the minds of everyone who knows what a remarkable human being you are

GH

Truth in science? We'll have none of that thankyou very much:

'According to emails and other documents obtained by Postmedia News in Canada, a scientist with Canada’s Department of Fisheries and Oceans (DFO), who was researching the reasons for the sudden decline of sockeye salmon in western Canada in 2007, was ordered by the government not to discuss the results of her study with members of the press.

Kristi Miller, head of the Pacific region’s molecular genetics section of the DFO, published her study in Science this past January, and as usual, the journal encouraged her to accept interviews with journalists about her findings. However, the Privy Council Office (PCO), which offers non-partisan advice to Canada’s Prime Minister, refused permission for Miller to conduct the interviews and also for the DFO to issue a press release.

In the study, Miller and colleagues conducted a genomic analysis of the fish and found increased expression in a set of genes associated with fighting infection or leukemia. While the researchers do not know the cause of the increased gene expression, they say that one potential source is a virus originating from fish farms.

The PCO claims that the reason for the denial is because the research is ongoing and that, next month, Miller is scheduled to testify before the Cohen Commission—a government task force set up to investigate the salmon decline. A spokeswoman for DFO said the department was concerned that interviews with Miller might sway the decision of the commission, reports ScienceInsider.'

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