Eric Fombonne
[back] Experts

When David Ayoub MD critically examined Fombonne’s Thimerosal claims and discovered the above facts (and many more), he reported them in a letter to the editor of PEDIATRICS. In return, he received a “form” e-mail stating that his letter could not be published because of lack of space. Later, a friend who inquired was told that that Dr. Ayoub’s letter was not published because “Dr. Fombonne did not wish to answer it.” [Sept 2008] The Unconvincing Thimerosal Epidemiological Studies: How and Why They Were Produced, Published and Protected by F. Edward Yazbak, MD, FAAP

The AAP has played an important role in perpetuating the misconception that current research refutes the thimerosal-autism link. Three key papers have been published in the AAP trade journal PEDIATRICS-Madsen (Danish epidemiological study); The Verstaraetn study, of Simpsonwood fame, and Fombonne (Quebec epidemiological study)
    The editor-in-chief Dr Jerald Lucey received numerous, substantiated criticisms of each of these studies, but has created an effective roadblock in disallowing any criticisms to be published in the letter-to the editor section of the journal. His response to thoughtful and reasonable criticisms has been unprofessional, illogical and insulting. My own letter to Lucey criticizing the Fombonne study was not even allowed to be published on the less publically visible online forum, even though we had obtained a copy of the Fombonne database and vaccine records from several parents proving Fombonne's work fraudulent. [2008] Dr Ayoub Speech at rally

[From: "Clifford G. Miller"  Dear Professor Leventhal]

[May 2007] The mercury, autism debacle: How stupid do they think we are? by Michael Wagnitz

http://www.mrw.interscience.wiley.com/cochrane/clsysrev/articles/CD004407/pdf_fs.html
Fombonne is a psychiatrist. Here is what the Cochrane Collaboration  said about Fombonne's last paper regarding a review of the safety of  the mmr:  "The number and possible impact of biases in this study is so high  that interpretation of the results is impossible".  (page 21) 

“E. Fombonne has provided advice on the epidemiology and clinical aspects of autism to scientists advising parents, to vaccine manufacturers (for a fee), and to several Government committees.” In plainer language, Fombonne had been a paid adviser to the manufacturers of MMR in the then-impending 1,500-strong class action High Court case in the UK that alleged that MMR had precipitated children’s degeneration into autism. The wisdom of using a paid witness to the manufacturers, as defendants, in a central authorship role in a supposedly independent research paper, might be questioned by many. --David Thrower

I was the first to announce the "autism epidemic", in 1995, and I pointed out in that article that excessive vaccines were a plausible cause of the epidemic.  As you know, an enormous amount of clinical laboratory research (as opposed to epidemiological research), has been accumulated since that time, supporting my position. (I did not know then that the vaccines contained mercury, although I had been collecting data since 1967 from the mothers of autistic children, on any dental work they may have had during their pregnancy.)  The evidence is now overwhelming, despite the misinformation from the Centers for Disease Control and Prevention, the American Academy of Pediatrics and the Institute of Medicine.------- The (Pretending to) Combat Autism Act  By Bernard Rimland

Professor Sir Michael Rutter along with a troupe of psychiatrists now or formerly associated with The Maudsley Hospital and The Institute of Psychiatry at Kings have been working hard at telling the public autism is solely genetic and denying there is a world autism pandemic.  .....Genetics cannot account for the large rise we are seeing in autism since the mid 1980s.  So instead what we see are efforts by Rutter and the King's Institute of Psychiatry other autism denialists to claim there is no real rise in the prevalence of autism.  This claim is unscientific and runs counter to the facts documented in the formal literature.
    The Institute of Psychiatry has or is home to more than its fair share of doctors (psychiatrists mostly) who publish papers claiming autism is genetic and denying there is an autism epidemic (the correct word is pandemic - epidemics have far fewer victims).  These doctors include Rutter, Eric Fombonne, (now expert witness in the US in the thiomersal/autism litigation when he had previously published nothing about it), Simon Baron Cohen.  It is also home to controversial "Gulf War Syndrome" psychiatrist Simon Wessely, director of the Centre for Military Health Research at King's College London and who had been claiming ME/CFS is not a physical condition but a mental one contrary to the definition used around the world...... Rutter was also an expert witness in Malmo, Sweden in an MMR autism case where the key question was whether autism was solely genetic and not environmental.  Rutter's expert evidence was that it was genetic.  Professor Sir Michael Rutter & The Drug Industry Connections

See: Urinary porphyrin profiles  Studies (government)   Studies on vaccine autism link

[2006 July 1] Pediatrics. "Pervasive Developmental Disorders in Montreal, Quebec: Prevalence and Links With Immunizations"--- Dr. Fombonne

[2004 Sept Lancet] "MMR Vaccination And Pervasive Developmental Disorders: A Case Control Study." By Liam Smeeth, Claire Cook, Eric Fombonne, Lisa Heavey, Laura C Rodriques, Peter G Smith, Andrew J Hall. Lancet 2004; 364:963-969.

• This was an important paper in that it claimed to have looked at a very large number of child health records, giving it considerable claimed authority. The study had been set up in the UK in the light of strong public concern (and probably a degree of internal UK Government unease) over the safety of MMR vaccination.
  Data were abstracted from the UK General Practitioer Research Database.
  The study found that:
• MMR vaccination was not associated with an increased risk of subsequent PDD diagnosis. The study found “no convincing evidence” that MMR vaccination increased the risk of autism or other pervasive developmental disorders
•  The “odds ratio” associated with MMR vaccination varied according to the age at which a person joined the GPRD. In particular, the odds ratio associated with MMR vaccination was higher among children who joined the GPRD at birth or before their first birthday. This was dismissed as possible selection bias or a “chance result”
• ·Research into the cause(s) of autism was urgently needed The study included over 1,000 cases with a diagnosis of PDD. Despite its size, the study had a number of drawbacks, some of which the study authors admitted:
•  some recording of previous vaccination history, where children came onto a GPRD after date of vaccination, was acknowledged to be possibly incomplete
• the study admitted that it was not able to separately identify the subgroup of cases with regressive symptoms, so as to be able to investigate the hypothesis that only some children were vulnerable to MMR-induced disease and that this was always regressive. This was a crucial failing, as this hypothesis lies at the very heart of the allegations of parents and the views of researchers such as Dr. Andrew Wakefield. On page 967, the authors stated that “we were not able to separately identify the sub-group of cases with regressive symptoms (so as) to investigate the hypothesis that only some children are vulnerable to MMR-induced disease and that this is always (in those cases) regressive”. The authors thereby are admitting that they have not, in fact, conducted an investigation of “the Wakefield hypothesis”
•  The study claimed that its results were similar to a Danish cohort study (the Madsen et al study). However, the use of thimerosalcontaining vaccines in Denmark has not matched that in the UK, and so comparing the two countries’ experiences may be inappropriate

The study also had to declare one serious conflict of interest, specifically that “E. Fombonne has provided advice on the epidemiology and clinical aspects of autism to scientists advising parents, to vaccine manufacturers (for a fee), and to several Government committees.”
In plainer language, Fombonne had been a paid adviser to the manufacturers of MMR in the then-impending 1,500-strong class action High Court case in the UK that alleged that MMR had precipitated children’s degeneration into autism. The wisdom of using a paid witness to the manufacturers, as defendants, in a central authorship role in a supposedly independent research paper, might be questioned by many.

This study was heavily criticised:

• the study is only epidemiological, not clinical. No children were examined
• the UK GP Research Database, the basis for this study, was not designed to be used for a study such as this
• there may have been some misclassification of cases (the authors admitted this flaw). In fact, it is understood that no fewer than 73 “controls” were discovered during the course of the study to be “cases”, illustrating the difficulty of relying on the GPRD database
• insufficient controls were used. Although the study, which used 1,294 cases and 4,469 controls, had initially indicated that there would be ten controls per autism case, 594 cases had fewer than three controls, 72 cases had only one control and 25 had none at all. It was not explained why the study’s original protocols had been apparently disregarded
• only 62% of the children had received MMR before 18 months. Yet the focus of concern needed to be on infants younger than this, 15 months or less. This makes the study less relevant to the core area of concern
• methodological flaws in the study were pointed out to the study team at early stages of the study, but do not seem to have been taken into account
• the study deliberately excluded children who did not have a record of seeing their GP in the 12 months prior to the “index date”, which was the date at which the children received a diagnosis of PDD. This could have increased the risk of excluding children who had undergone definite regression after MMR

Comment: this study cannot be taken as offering reliable evidence to deny an MMR/autism link, despite the claims made at the time. It is worth reminding readers as to the original “Wakefield hypothesis”, as published in the Israeli Medical Association Journal, 1999, Volume I, pp1-5: “There exists a subset of children who are vulnerable to developing a particular form of regressive autism following previously normal development, in combination with a novel form of inflammatory bowel disease. Onset may occur over weeks or sometimes months, and is triggered by exposure to a measles-containing vaccine, predominantly the measles mumps rubella vaccine (MMR) that is in use in much of the world today. This exposure leads to long term infection with measles virus within key sites, including the intestine where it causes inflammation.”

[pdf March 2006] MMR Vaccine, Thimerosal and Regressive or Late Onset Autism A Review of the Evidence for a Link Between Vaccination and Regressive Autism--David Thrower

[Sept 2004] Dr. Wakefield Responds To British Study Clearing MMR Vaccines

[2004 Nov] Study by Smeeth, Fombonne, Hall et al. Rate of First Recorded Diagnosis of Autism and Other Pervasive Developmental Disorders in United Kingdom General Practice, 1988 to 2001 published in BMC Medicine, 2: 39, November 2004.
This study analysed the rates of first diagnosis of pervasive developmental disorders amongst people registered with GP practices that were part of the UK GP Database during 1988-2001. It included 1,410 cases drawn from over 14 million person-years of observation. The main outcome measures were the rates of diagnosis of PDD, by the year of diagnosis, the year of birth, by gender and by geographical region.
The study found that:
· the rate increased progressively from 0.40/10,000 person years in 1991 to 2.98 per 10,000 person years in 2001
· there was a similar increase in standardized incidence ratios, from 35 in 1991 to 365 in 2001
· the temporal increase was not limited to children born during specific years, nor to children diagnosed in a specific time period
· the rate of diagnosis of PDDs other than autism rose from zero for 1988-92 to 1.06 per 10,000 person-years in 2001
· the rate of diagnosis of autism also increased, but to a lesser extent
· there was marked geographical variation in rates, with standardized incidence ratios varying from 66 in Wales to 141 for SE England
The study concluded that better ascertainment of diagnosis was likely to have contributed to the observed temporal increase in rates of diagnosis of PDD, but the authors could not rule out a real increase. The study claimed to be on of the largest undertaken of trends in the incidence of autism
The study authors had to admit to a considerable number of uncertainties, and make a number of suppositions. Uncertainties included:
· it was “likely” that a proportion of cases in the “autism” diagnostic category had a form of PDD other than autism
· the inaccuracy of diagnosis within the GP research database was “likely” to reflect changes in the definition of PDD
· inflation in the number of cases in later years “could have” occurred as other PDD diagnoses came into widespread use and some previously-undiagnosed children were diagnosed
· greater ascertainment of high functioning autism “may partly explain” the increased incidence of autism
· better detection of less severe cases alone cannot explain all the increases
· geographical variation “may” reflect differences in service provision and parental awareness in different regions
· the accuracy of the data “may” have changed during the study period
· these factors “could explain only a very small part” of the increased rates observed
· the nature of the study precluded the authors from assessing how often children with PDDs were not diagnosed
The study team concluded that the extent to which the increase in incidence that were documented was uncertain.
Comment - there are many criticisms that can be made of this study, many of which are identified by the study team themselves as potential confounding factors.
The study clearly found large increases, and attempted to shrug these off by linking them to factors such as better diagnosis and greater awareness. However, it was unable to accurately weigh these factors and quantify their individual influence. It is therefore the case that the study has very limited value. It is again interesting that the study authors seem anxious to avoid reaching the conclusion that there has been a large real increase in autism. [pdf March 2006] MMR Vaccine, Thimerosal and Regressive or Late Onset Autism A Review of the Evidence for a Link Between Vaccination and Regressive Autism--David Thrower

[2003 Jan] Fombonne, editorial, Journal of the American Medical Association, January 1st 2003 Vol 289, No.1 49

At the start of 2003, Dr. Eric Fombonne wrote an editorial in the Journal of the American Medical association that appeared to acknowledge that there had been some real increase in autism, but which also attempted to explain this away to as great a degree as possible through the usual recourse to references to better awareness, less restrictive criteria and a greater willingness to diagnose.
Fombonne’s key points were that:

• That the prevalence rate of 34 per 10,000 (1 in 294) was likely to actually be an underestimate, because high-functioning autism cases were likely to have been missed.
• The lower reported prevalence in 3- and 4-year olds might reflect lower sensitivity of case identification for disorders, which were often diagnosed later
• There was an unexpected decrease in prevalence amongst 9- and 10-year olds. Fombonne dismisses the idea that this might imply that the younger the birth cohort, the greater the level of autism as being “biologically implausible”. Yet this is open to obvious question - what if an external factor had altered during this time? Fombonne does not address this possibility.
  Fombonne concluded that a rate of 41-45 per 10,000 (1 in 222) might be a more accurate rate of prevalence. He noted in his editorial that other studies suggested rates of 60 per 10,000 when pervasive developmental disorder-not otherwise specified (PDD-NOS) and Aspergers syndrome were taken account of.
  He then addressed the issue as to whether the prevalence of autistic spectrum disorder (ASD) had increased over time. His benchmark was the 1970s Wing and Gould study in Camberwell, London, which pointed to a rate of 20 per 10,000 for severe-impairment cases. Other earlier studies had point to rates of 4 or 5 per 10,000, and more recent studies cited by Fombonne pointed to rates of more than 10 per 10,000. Fombonne’s conclusion was that the most recent rates of prevalence were three or four times higher than 30 years ago.

Fombonne, seemingly searching for an uncontroversial explanation for any increase, then examined whether this increase implied a broadening of criteria and improved methods of case-finding during studies. He pointed to what he described as the “major” changes in criteria:

• Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III), 1980
• DSM Revised Third Edition (DSM IIIR), 1987
• DSM Fourth Edition (DSM IV), 1994.

He argued that there was strong evidence that differences in methods for case finding could account for a “huge” proportion of the variability of prevalence estimates between surveys. Referral rates were also unreliable, due to confounding factors. This, and other factors, he concluded, combined to offer “good” evidence to support the contention that higher rates of prevalence reflected changes in diagnostic practice, improved identification and availability of services. The hypothesis of an increasing trend in the incidence of autism could not, in his view, be fully tested because of the inadequacy of studies to date. Fombonne dismissed any association with MMR (citing his own study work and studies by Madsen and by Taylor and Miller as proof), and dismissed evidence of any connection with thiomersal as being “weak”.

Fombonne was also quoted in the New York Times of 31st December 2002 as stating: “No strong candidate environmental exposures have been identified.....Claims of an association with MMR have not been borne out by recent studies, and evidence for causal association with other exposures such as mercury-containing vaccines is weak”.

The study being commented on by Fombonne was that by Dr. Marshalyn Yeargin-Allsop et al, detailed earlier. Comment: the editorial by Fombonne offers no hard evidence against a vaccine/autism link, and, whilst offering some arguments in favour of questioning the precise scale of the apparent major rise in autism prevalence, fails to demolish the central assertion of many parents, that autism has grown immensely in a couple of decades. No alternative explanations for the rise are offered by the Fombonne editorial. [pdf March 2006] MMR Vaccine, Thimerosal and Regressive or Late Onset Autism A Review of the Evidence for a Link Between Vaccination and Regressive Autism--David Thrower

[2001 Oct] Fombonne & Chakrabarti, No Evidence for a New Variant of Measles-Mumps-Rubella-Induced Autism, Pediatrics, Vol. 108 No. 4 October 2001

This paper examined whether there is a new phenotype of autism involving regression and gastrointestinal symptoms.
It is suggested that where this paper is flawed is in the assumptions underpinning the hypotheses that are tested. All else stems from that.
Fombonne & Chakrabarti assume that if autistic enterocolitis existed, then one or more of the following six predictions should be supported by empirical data:

• Prediction (1) - “childhood disintegrative disorder has become more frequent”. (The study found the prevalence of childhood disintegrative disorder to be 0.6/10,000, or 1 in 16,666. But this seems far too low in comparison with other recent studies).
  Comment - historic data is not available to prove this either way. The claim that the present rate of 1 in 16,666 represents no increase is further undermined by its non-credible low level. Other studies have found rates very many times higher. This strongly suggests that the study is flawed.
• Prediction (2) - “the mean age of first parental concern for autistic children who are exposed to MMR is closer to the mean immunisation age than in children who are not exposed to MMR.”
  Comment - the study found that there was no difference in the mean age at first parental concern between the two samples exposed to MMR (19.3 months and 19.2 months) and the pre-MMR sample (19.5 months). But no argument has been presented as to why there should be a difference. A difference might be expected, but its absence in itself does not prove anything. It is perfectly possible that childhood disintegrative disorder has several causes, and that the arresting of development could be noticed at around the same time. Pre-MMR children who became autistic may well have become so due to an adverse outcome from monovalent measles vaccine. This possibility does not seem to have occurred to Fombonne. There is also a simplistic focus upon MMR alone as a sole factor, working in isolation, rather than as part of a complex process.
• Prediction (3) - “regression in the development of children with autism has become more common in MMR-vaccinated children.” The study found that the rate of developmental regression reported in the post-MMR sample (15.6%) was not different from that in the pre-MMR sample (18.4%) and therefore there was no suggestion that regression in the development course of autism had increased in frequency since MMR was introduced. The study also found that in the epidemiologic sample, the subset of autistic children with regression had no other developmental or clinical characteristics, which would have argued for a specific etiologically distinct phenotype.
  Comment - the samples were small. The study used three samples, a post-MMR sample of 96 children with PDD, a pre-MMR sample of 98 autistic patients, and a post-MMR sample of 68 autistic patients. These are very small numbers to use in a statistically-based study. Fombonne and Chakrabarti’s results should thus be treated with caution, as a few cases either way would impact upon their conclusions.
• Prediction (4) - “the age of onset for autistic children with regression clusters around the MMR immunisation date and is different from that of autistic children”. The study found that parents of autistic children with developmental regression detected the first symptoms at a very similar age (19.8 months) to those of autistic children without regression (19.3 months). The study also found that the mean intervals from MMR immunisation to parental recognition of autistic symptoms were comparable in autistic children with or without regression (248 days vs 272 days, not significant).
  Comment - but regression might not necessarily be expected to “cluster round”, but may follow MMR at a delay of weeks, months or years. There is no scientific justification for assuming that children with regression after MMR should have their condition recognised at a different time to those who did not regress after MMR. In any event, it is stated that the difference between 248 days and 272 days is not significant, but it is almost 10% different, and this difference has not been explained.
• Prediction (5) - “children with regressive autism have distinct symptoms and severity profiles.”
  Comment - little scientific justification for testing this assumption is given in the study, which also refers to external features such as behaviour, when the real focus of interest should be on gut biopsies and ileocolonoscopies of the actual children, which of course were not done in this study. Not enough is known about autistic enterocolitis to make such an assumption about external characteristics into a key test.
• Prediction (6) - “regressive autism is associated with gastrointestinal symptoms and/or inflammatory bowel disorder”.
  Comment - but the children in this study did not undergo ileocolonoscopy.
  Their condition was medically unresearched.
  Other comments:
• this is a statistical analysis of random groups of children, not of the children whose cases are going to the High Court. The numbers are extremely small, too small for a reliable interpretation to be made
• The assumption seems to have been made that children could not have been damaged by vaccines other than MMR. The Lassiter court case outcome (US) means that there is evidence, that has been accepted in a Court that other multiple vaccines also trigger autism.
• What this study set out to do was not to investigate the cause(s) of damage to specific children, but to clear MMR of any complicity. At first sight, it succeeds in the latter, but at closer analysis, it makes numerous unfounded assumptions that considerably weaken the strength of its conclusions. At worst, it demonstrates the central flaw of designing a study hoping to achieve a desired outcome, rather than to investigate a problem.
  Overall verdict: this study fails to provide any convincing evidence against an MMR/autism link.
  (Note: this study has been claimed by the UK Medical Research Council to represent “strong positive evidence” of there being no MMR/autism link)

[pdf March 2006] MMR Vaccine, Thimerosal and Regressive or Late Onset Autism A Review of the Evidence for a Link Between Vaccination and Regressive Autism--David Thrower

[2001 Jan] Paper by Fombonne, Medical Research Council Child Psychiatry Unit and Institute of Psychiatry, Is There An Epidemic of Autism?, Pediatrics, January 2001

 At the end of January 2001, a paper, “Is There An Epidemic of Autism?” was published by Dr. Eric Fombonne. The paper sought to deny that autism had really increased, and criticised the “poor research methodology” of Dr. Andrew Wakefield, and said “There is no need to raise false alarms on putative epidemics nor to practice poor science.....”

 ?         Fombonne criticises the California increase on the basis of in-migration, possible changes within the population make-up, the change from DSM-III to DSM-IIIR in 1987, the introduction of diagnostic categories for Asperger, Rett and childhood disintegrative disorder in DSM-IV in 1994, the effects of earlier diagnosis adding to the totals, and other factors.

 ?         His most useful conclusion is that “we simply lack good data”. He raises doubts about the apparent epidemic, but is then unable to refute it either.

 In an excellent FEAT (parents’ group) critique (8th Feb 2001), Mark Blaxill goes carefully through Fombonne’s previous work and argues that Fombonne has become inconsistent. He points out key flaws in Fombonne’s previous work, and criticises his criticisms of the California data and his scientifically-unsupported assertions [July 2004] MMR and Acquired Autism (Autistic Enterocolitis) - A Briefing Note by David Thrower

[2000-2002 Unpublished Study by Fombonne et al, A Case-Control Study of Autism In General Practice, UK, Study Period September 2000-August 2002

 This study, based at the Maudsley Hospital, Denmark Hill, London, is to assess if exposure to MMR immunisation is a risk factor for autism, and to assess the exposure to viral infections, both prenatally and postnatally. Despite the dates, as far as is known the study has yet to report.

 The study will use UK GP data, hospital reports and a parents’ questionnaire. It will use over 400 cases of autism and four times as many controls, selected from a GP database. It is funded by the Medical Research Council (£351,000). No date has been given for publication of the findings.

 (Note: since this study commenced, Professor Fombonne has also agreed to appear at the forthcoming UK High Court cases as an expert witness on behalf of the manufacturers of MMR, against the children. His current role within the study is not known. It is also not known whether the control group will be “unvaccinated with MMR”, “unvaccinated with MR”, “unvaccinated with any measles-containing vaccine”, “unvaccinated with thiomersal-containing vaccines” or “totally unvaccinated”, or what the vaccination status of the control group children’s mothers will be. These may affect any study findings). [July 2004] MMR and Acquired Autism (Autistic Enterocolitis) - A Briefing Note by David Thrower

[1998] Letter by Dr. Eric Fombonne, Inflammatory Bowel Disease and Autism, Pediatrics, March 28th 1998

 This letter set out two studies that attempted to prove that there was no connection between inflammatory bowel disease/Crohn’s disease and autism. The first study looked at UK clinical data collected by the Child & Adolescent Psychiatric Services of the Maudslay Hospital, London.

 ?         For ASD, three diagnostic groups were examined, autism, atypical autism including disintegrative disorder, and pervasive developmental disorder

 ?         Medical disorders were coded for a 25-year period, including Crohn’s and ulcerative colitis, for 8889 patients.

 ?         Of the 8889 patients, 987 were born in 1987 or later, and were therefore most likely to have been exposed to MMR. Of these, 201 had ASD.

 ?         Of the 8889 children, only two had Crohn’s, and both were non-autistic. None had ulcerative colitis.

 For the second study, a similar approach was undertaken. Fombonne surveyed medical, behavioural and intellectual disabilities amongst 6100 French children.

 ?         He found 174 cases with autism.

 ?         One child of the 6100 had Crohn’s, and one had ulcerative colitis. Neither were autistic

 ?         The conclusion that Fombonne drew was that these data provide no support for the hypothesis of an association between IBD and autism. 

 Overall verdict: neither of these studies offer any evidence to disprove an MMR/autism link. [July 2004] MMR and Acquired Autism (Autistic Enterocolitis) - A Briefing Note by David Thrower