Beyond Our Ken
Ken Aitken is a clinical psychologist who co-authored a text book on autism. (Trevarthen et al. 1996). The book acknowledges that rubella in pregnant women is a cause of autism but notes that, “greater awareness of the disorder and widespread inoculation have virtually eradicated rubella as a significant cause of autism.” (page 91)
Five years later Aitken appeared as an expert witness before an enquiry into the safety of MMR vaccine called by the Scottish parliament. But instead of supporting a vaccine that had helped to eliminate “a significant cause of autism” he supported the connection between the MMR vaccine and autism. He specifically rejected the suggestion that mercury might be to blame in the UK because, compared to the USA, there are negligible amounts of mercury in our vaccines. (Aitken 2001)
So, when Aitken addressed the Treating Autism Conference in Edinburgh, held on 14 - 15 October 2005 I was surprised to see a slide attacking mercury in his presentation. (Aitken 2005) Has the amount of mercury in our vaccines suddenly increased? Is Aitken a mercury convert because the case against MMR has collapsed? Or was he playing to the gallery because he knew that his audience was sympathetic to the mercury hypothesis?
Whatever the reason, his present position is in marked contrast to the views expressed in his book. Then he argued that, “It now seems certain that the brains of person’s who became autistic in their early childhood already had microscopic faults in their development in early intra-uterine life, probably expressed among cells of the early embryo, in the first month.” (page 80)
Now he argues that
There is a dramatic increase in autism that is caused by new forms of autism that occur in normally developing children who regress after an environmental insult in early childhood.
Regressive autism now dwarfs other forms of autism.
Is there an increase in numbers?
More and more people are being diagnosed. But as early as 1979 the Camberwell Study suggested that autism was far more prevalent than people had previously thought. It found rates around 20 in 10000 in children with learning difficulties. (Wing and Gould 1979). This is identical to the prevalence rate in California that is cited as evidence for an “autism epidemic” In the 1990s.
“The cumulative prevalence of autism in California increased from 7.5 per 10,000 for the sample 1983-85 birth cohort to 20.2 per 10,000 for the 1993-95 birth cohort, an increase of 269 percent.” (CDDC 2003)
Scotland is the one part of the United Kingdom where there is a system in place for recording all known cases of autism. Aitken acknowledges that if we accept official estimates of a prevalence rate of 60 in 10000 only 44% of cases are diagnosed. (PHIS 1991) So what is going on? A diagnostic rate of 26 in 10000 in Scotland is evidence of under diagnosis. A diagnostic rate of 20 in 10000 in California is evidence of an epidemic.
Is there an increase in regressive autism?
Aitken believes that cases of regressive autism have “grown to dwarf those with more ‘typical’ presentations.” Published research shows that the proportion of cases of regressive autism have not changed. (Taylor, Miller, Lingam, Andrews, Simmons & Stowe 2002. (page 394))
Aitken knows this because he cites the same paper as evidence of a link between bowel problems and regressive autism.
“…bowel problems were reported more frequently in children with regression than in those without, 31 of 118 (26%) and 49 of 351 (14%) respectively (P = 0.002).”
Though it would have been more honest to quote the whole paragraph:
“Although neither bowel problems nor regression was related to MMR vaccination, bowel problems were reported more frequently in children with regression than in those without, 31 of 118 (26%) and 49 of 351(14%), respectively (P = 0.002). This relationship between bowel problems and regression did not significantly vary by type of bowel problem (P = 0.35).
For the 31 children with both bowel symptoms and regression, there was also no association with MMR vaccination (P = 0.20) and no association with year of
birth (1.01, 0.92 to 1.11; P = 0.79).”
Taylor, Miller, Lingam, Andrews, Simmons & Stowe 2002. (page 395)
Much of the evidence for regression comes from parental reports. And it is not always clear whether they are reporting regression or failure to meet expected milestones. It is also necessary to exercise caution when dealing with parental evidence. Aitken knows this. It is in the same study by Taylor et al.
“ A review of each record showed that in 13 children the history given by the parents had changed after the extensive publicity about MMR vaccine and autism. Before the publicity the parents often reported concerns early in their child's life, usually before their first birthday; the current history for the same children recorded symptoms as developing only after MMR vaccination, in some cases shortly after.”
(Taylor, Miller, Lingam, Andrews, Simmons & Stowe 2002. page 395)
So, Aitken has taken research that contradicts his previous position on the connection between MMR, bowel problems and regressive autism and selectively quoted from it to support his view that there is a connection between bowel problems and regressive autism, while ignoring the authors’ qualifying remarks about the reliability of parental memories concerning regression. There’s more. Aitken misrepresents a pilot study for a screening checklist as if it were an authoritative measure of autism incidence among 18 month old children. (Baird G, Charman T, Baron-Cohen S, Swettenham J, Wheelwright S, Drew A 2000)
This study successfully predicted autism in 10 subjects out of 16,235 children but failed to identify a further 40 autistic children. Finding 6 in 10000 out of an actual incidence of 30 in 10000 in a particular birth cohort does not prove that the other children are victims of regression. This was a just pilot study for a screening test, not a full scale case finding exercise using the latest diagnostic techniques. Aitken uses it to support his thesis that regressive autism dwarfs traditional autism. What utter nonsense!
These are just a few of the problems I have with Aitken’s presentation. Another feature of his theory is that if there is a new form of autism there has to be a really low rate of autism in populations born prior to the alleged autism epidemic. Aitken uses these sources as proof.
Burd and colleagues in North Dakota estimated 3.26 per 10,000 in those born between1967 and 1983 (Burd, Fisher & Kerbeshian 1987; Burd, Kerbeshian, Klug &McCulloch 2000). In Sweden, Nylander and Gillberg (2001) found a prevalence rate of 2.7 per 10,000, screening previously
undiagnosed adult psychiatric outpatients.
The problem is that Burd (1987) was using DSM III criteria that were highly restrictive compared to the present DSM IV(R) criteria. There is an interesting discussion about diagnostic criteria, autism epidemics and the perils of comparing prevalence rates over time that Aitken ought to read (Medscape 2005)
The second study by Burd et al. was actually a follow up to assess the methodology used in the original study and using the same methodology the authors found another autistic individual whom they had missed in 1987. This was not a study to assess the prevalence of autism in North Dakota in 2000.
The study by Nylander and Gillberg (2001) actually found
“at least 19 patients in this population (1.4%) had a definite ASD. Seventeen of the ASD patients had been previously diagnosed with other psychiatric disorders, most frequently schizophrenia (n=5). Of patients attending a treatment centre for severe psychiatric disabilities (n=499), 3.2% had an ASD.”
So where did Aitken find his figure of 2.7 per 10,000? Perhaps he reads the British Medical Journal. Mark Blaxhill, a board member of Safe Minds, the acronym for the snappily named Sensible Action For Ending Mercury-Induced Neurological Disorders. Blaxhill wrote to the BMJ citing these same three references as proof that there was no “hidden horde” of previously undiagnosed adults.(Blaxhill 2002) Has Aitken read any of the studies he cites or does he just accept the citations given to him by the “mercury moms” and their supporters?
Aitken 2001 http://www.show.scot.nhs.uk/mmrexpertgroup/Aitken-rep.htm
Aitken 2005 http://www.actagainstautism.org.uk/presentations/14th/aitken.pdf
Baird G, Charman T, Baron-Cohen S, Swettenham J, Wheelwright S, Drew A (2000) A screening instrument for autism at 18 months of age: a 6-year follow-up study. Journal of the American Academy of Child and Adolescent Psychiatry, 2000 Jun, 39(6):694-702
Blaxhill 2002) Letter to the editor. British Medical Journal Volume 324 2 February 2002 page 296
Burd L. Fisher W. Kerbeshian J. (1987) A prevalence study of pervasive developmental disorders in North Dakota. Journal of American Academy of Child and Adolescent Psychiatry, 1987, Vol. 26(5), pp. 700-703
Burd L, Kerbeshian J, Klug MG, McCulloch K. (2000) A prevalence methodology for mental illness and developmental disorders in rural and frontier settings. Int J Circumpolar Health. 2000 Jan;59(1):74-86.
CDDC (2003) AUTISTIC SPECTRUM DISORDERS Changes In The California Caseload An Update: 1999 Through 2002
Medscape 2005 http://www.medscape.com/viewarticle/508429
MRC (2001) http://www.mrc.ac.uk/pdf-autism-report.pdf
Nylander L. Gillberg C. (2001) Screening for autism spectrum disorders in adult psychiatric out-patients: a preliminary report. Acta Psychiatrica Scandinavica, 2001, June, Vol. 103 (6), pp. 428-434
PHIS (1991) Autistic Spectrum Disorders Needs Assessment Report
Taylor, Miller, Lingam, Andrews, Simmons & Stowe (2002) Measles, mumps, and rubella vaccination and bowel problems or developmental regression in children with autism: population study British Medical Journal, 2002, Vol. 324, pp. 393-396
Trevarthen, C., Jacqueline Robarts, J., Despina Papoudi, D. and Aitken, K. (1998) Children with Autism Diagnosis and Intervention to Meet Their Needs. Jessica Kingsley Publishers London.
Wing, L. & Gould, J. (1979). Severe impairments of social interaction and associated abnormalities in children: epidemiology and classification. Journal of Autism & Developmental Disorders, 9, pp. 11-29.