Vaccines and autism: a thoughtful debate 1

I have just started watching the video of the debate between David Kirby and Arthur Allen on the subject of autism and vaccines. Kirby wrote a book, Evidence of Harm: Mercury in Vaccines and the Autism Epidemic: A Medical Controversy which starts from the premise that the rapid growth in recorded cases of autism in the USA that began in the early 1990s represented a real growth in numbers and could not be explaind by increased awareness, better diagnostic procedures or a change in the criteria. There had to be an environmental trigger. At the same time changes in the mandatory vaccination programme for children in the USA  increased exposure to thimerosal, a preservative that contains ethyl mercury.  

Did the thimerosal cause an autism epidemic? Kirby believes it did. Allen once thought it was a credible hypothesis. But in the course of researching his book, Vaccine, the Controversial Story of Medicine’s Greatest Lifesaver, Allen changed his mind.  Allen has also begun to question whether there has been an epidemic or not. See his review of Roy Grinker’s book, Unstrange Minds, Remapping the World of Autism. 

I was looking forward to the debate. But within minutes I was hitting the pause button and diving into my archive of autism related papers. Kirby began, quite rightly, with a discussion of epidemiology. But his version seemed at odds with what I thought I knew. Still, this was an important debate. Kirby must have checked his facts beforehand. So I went to check mine.

Kirby’s Fact 1.

In the 1980s autism prevalence in the USA was between 1 and 2 in 10,000

If anyone has a reference to an epidemiological study for this extremely low figure I would love to have it.  When Lorna Wing surveyed the major epidemiological studies carried out between 1966 and 1992 she referred to two studies in Utah (Ritvo et al 1989) and North Dakota (Burd et al 1987) that found rates of 4 and 3.3 in 10,000 respectively for DSM III autism which use very similar criteria to Kanner’s criteria. She also mentioned a study by Treffert which found a prevalence of 3 in 10,000 in 1970 in Wisconsin. When I considered Wing’s survey in an earlier post  I remarked upon the robust nature of the figures. Researchers who combined consistent epidemiological methods with Kanner’s diagnostic criteria found rates of between 4 and 5 in 10,000.

Kirby’s Fact 2.

In the late 1990s autism prevalence in the USA was 20 in 10,000

Kirby offers no citations for this figure. Probably the most well founded study in the USA in the 1990s was by Yeargin-Allsopp et al in Atlanta in 1996 which found a rate of 34 in 10,000 in 3-10 year olds. It was reprinted in JAMA in 2003. In the same edition Fombonne considers this an underestimate and thinks the 5 to 8 year olds in the study provide a more reliable estimate of 41 – 45 in 10,000. (JAMA 2003 Volume 289 Issue 1.)For comparison Wing and Gould found a rate of 20 in 10,000 in the Camberwell study in 1979. This study confined itself to children with learning dificulties in special schools and never looked at children in mainstream classes where most autistic children are found today.

Kirby’s Fact 3.

By 2000 autism prevalence in the USA was 40 in 10,000

Again there is no citation. And autism prevalence in whom? What is the age cohort?

Kirby’s Fact 4.

By 2004 autism prevalence in the USA was 60 in 10,000

We do have a lot of epidemiology for this figure.It is supported by the Medical Research Council in the UK and the Centers for Disease Control in the USA. But it is usually taken to mean that we have now reached a reasonably accurate estimate of prevalence figures for the entire autistic spectrum across the entire population. Kirby sems to be using these figures to suggest a year on year increase in incidence which is not the same as prevalence. Generation Rescue made a similar mistake last year which I commented on.

When you are dealing with statistics it is important not to get incidence and prevalence muddled up. Incidence refers to the number of new cases in a population over a period of time. Prevalence refers to the total number of cases in a given population at a specific time.

Kirby’s Fact 5.

By 2004 th USA figure of 60 in 10,000 was the same as in the UK. But the USA had 40 in 10,000 with autstic disorder and only 20 in 10,000 with other ASDs. In Britain the figures are reversed: 20 in 10,000 with Autistic disorder and 40 in 10,000 with other ASDs.

Kirby’s explanation is simple. Here in the UK we only ever had half the thimerosal in our vaccines compared to our American cousins. So we only got half the autistic disorder. OK. Thimerosal causes autistic disorder. There is a linear relationship. Double the thimerosal and you double the autistic disorder. So what causes PDD-NOS and Asperger Syndrome? Why should they be twice as prevalent in the UK as in the USA? Is that environmental or genetic? Perhaps we Brits are naturally more high functioning than the Yanks 🙂

By this time I was beginning to get a little bit sceptical about Kirby’s figures. He actually did mention a source for his 40 in 10,000 with autistic disorder, Brick Township. I remember that one; 40 in 10,000 for autistic disorder is correct. But the figure in Brick Township for other ASDs was not 20 in 10,000. it was 27 in 10,000. 67 in 10,000! That is a lot of autism, except for one fact. It was a very small sample; 60 children aged 3 to 10. The authors acknowledge the problems in generalizing from their data.

As mentioned earlier, the major limitation of this study was an inability to ascertain higher functioning individuals who were not in any special education class in public schools or had not been seen by participating clinicians. Consequently, because of these case-finding limitations, the results from Brick Township must be considered a minimal prevalence for autism. Categorical distinctions between autistic disorder and the other ASD were probably limited because the ADOS-G has been found to over estimate autistic disorder relative to PDD-NOS. Also, because clinical assessments could not be conducted for 17 children and the diagnosis had to be based on records alone, the reliability and validity of the diagnosis for those children is limited. Discrimination between PDD-NOS and autistic disorder also may have been influenced for these cases given that over 56% of the children who participated in the clinical assessment were determined to have autistic disorder in comparison to only 27% of the children assessed by record review only. Finally, the prevalence rates for autism obtained in this study must be generalized with caution since the community was selected for study because of a suspicion of increased numbers of children with the disorder. Studies of larger populations, such as one that included surrounding communities, may yield different findings.

They may indeed.

Kirby’s Fact 6

Denmark removed all its thimerosal way back in 1992 and it has a rate of only 8 in 10,000.

Yes, except that according to this study autism rates went up in Denmark after they removed the thimerosal. Actually the base rates for autism in this study were so low it is ridiculous, less than 1 in a 1000 throughout the seventies and eighties. That is less than Brask found in 1972 in Denmark for Kanner’s autism. (4.3 in 10,000) A more recent study suggests the real rate for ASDs in Denmark is closer to the 34 in 10, 000 that Yeargin-Allsopp found in Atlanta in 1996. the authors conclude:

We found that the estimated prevalences of the PDDs studied were probably underestimated. Furthermore, the increasing prevalence and incidence rates during the 1990s may well be explained by changes in the registration procedures and more awareness of the disorders, although a true increase in the incidence cannot be ruled out.

So much for Denmark then. I cannot say that  I am looking forward to the rest of this debate if this is the standard of evidence employed by Kirby. But I will resist the temptation to fast forward to Arthur Allen. I will do my blogging duty. Speaking of Arthur Allen, he has written about the debate on his blog and is open to comments. Kirby, despite boasting that whenever he writes on the Huffington Post he goes straight to number one, has yet to share his thoughts on the debate with a wider audience.

 STOP PRESS Kirby has made the slides  from his presentation available on his website. I wont be downloading them just yet. I don’t want to spoil the ending.

to be continued …

EDIT

… or not. Kev has blogged the debate here and here. So has Joseph, BC and D0’C. And Diva has set it to music.

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Biomedical interventions in autism – a reply

The Winter 2006 edition of Communication, the quarterly magazine of the National Autistic Society contains an opinion piece, “Biomedical Interventions in Autism” by Lorene Amet. Unless otherwise indicated all quotes are from Amet’s article.

She claims that,

“A previously rare childhood developmental condition seems to have become common in ten years! This does not seem to be a matter of changing definitions, ascertainment bias, or case-finding methods. What this may tell us is that the role of environmental factors in autism is greater than previously envisaged.”

But according to a National Autistic Society leaflet, (NAS 1997)

“The best estimates of the total prevalence of autistic spectrum disorders are those based on the Camberwell and Gothenburg studies, because these focused on the whole spectrum and not just specific sub-groups.”

The Camberwell study (Wing and Gould 1979) found a prevalence of 20 in 10000 for autistic spectrum disorders amongst children with IQ less than 70. The Gothenburg study (Ehlers and Gillberg 1993) found a prevalence of 71 in 10000 for autistic spectrum disorders among school children with an IQ greater than 70. These studies were published in 1979 and 1993 respectively. So, when every newspaper and magazine report seems to include the obligatory statistic that, “1 child in 166 is now affected by autism,” we should remember that back in 1993 some of the leading autism experts in Europe were arguing that 1 in 110 children were affected then. One of their most trenchant critics, Eric Fombonne (1997) carried out his own epidemiological studies (Chakrabarti and Fombonne 2001, 2005)) which went a long way to confirming Wing and Gillberg’s position.

I fail to see the point of Amet’s remark “the explosion of autism diagnosis throughout the developed world continues to throw an uncomfortable light on the traditionalists within the autism community,” when, in fact, the explosion only serves to confirm what the traditionalists established during the 1990s, that when autism is understood as a broad spectrum disorder it is more prevalent than was suggested by previous studies that focused on the narrow portion of that spectrum first described by Kanner (1943).

Whether there has also been an increase in actual numbers alongside the increase in diagnosis is unknown. Fombonne (2003) argues that the few incidence studies we have are inadequate to the task. He also points to the extreme weakness of the evidence in support of a new environmental influence that might explain any secular incidence in autism in recent years. Amet is equally tentative about possible causes.

“32 reports … suggest that it [heavy metal toxicity] could be implicated.” There is a “possible association with autism” for “diet and food sensitivity; profound vitamin, minerals and fatty acid deficiencies; some abnormalities in purine levels and essential amino acid levels; as well as some cases with hormonal or cholesterol metabolism abnormalities.”

The one study she cites goes to show how tentative those links are. The Vargas paper (2005) is inaccurately reported as a study of “11 post-mortem brain tissues of children with autism.” These ‘children’ ranged in age from 5 to 44 years. If there is active neuroinflammation in subjects born in the 1960s it is unlikely that a recent, epidemic inducing toxin is responsible. And, far from proposing a “key pathological role in autism” as suggested by Amet, senior author, Carlos A. Pardo-Villamizar cautiously points out in a press release (Science Blog 2004) that, “it is not yet clear whether [the immune activation] is destructive or beneficial or both.” On the question of treatments he says that “much more research would be needed to establish the validity of this approach.”

Amet is not so tentative about possible treatments. Apparently, ‘could be’ and “possible association” provide sufficient proof to justify the treatment protocol on offer at her Edinburgh clinic. She agrees “that there is at present insufficient published evidence for the efficacy of the biomedical approach beyond anecdotal reports.” In plain English that means that there is no published evidence apart from anecdotal reports.

Amet believes it would be unethical to carry out proper research before experimenting on children because,

“the biomedical treatments that some feel have been shown to lead to recoveries are complex, comprised of several inter-dependent parameters, and carried out over a long period of time, usually for a minimum of two years.”

So studies on mice, monkeys and in vitro are good enough to suggest treatments but those treatments cannot be subject to clinical trials. This is quackery pure and simple. Amet argues that,

“It is only through thorough examination and biomedical testing that the individual child’s symptoms can be understood and treatments tailored accordingly.”

Autism is presently only diagnosable on the basis of observable behaviours. Amet would like to be able to diagnose on the basis of biomedical indicators. But here she suggests that it is already possible to match autistic symptoms to biological markers.

Once these biomedical problems are identified they will be treated with dietary and pharmaceutical interventions that will also cure the autistic symptoms. Biomedical interventions are often used in conjunction with applied behavioural analysis on the premise that the child needs to be re-educated in what it is to be normal while they are being recovered from their autism.

Quite aside from the arrogance that presumes such knowledge of the biochemical predictors of behaviour and competence to manipulate them successfully, there is the complete denial of any autonomy for the child in determining who they are. The child is a tabula rasa with no opportunity for influencing the outcome of their own development and education.

While every child is different,

“children with autism have a set of characteristic clinical complaints. And these are very well-substantiated in the current peer-reviewed medical and scientific literature.”

It would help if Amet could provide a list of these “characteristic clinical complaints” and some reference to the relevant literature. In contrast to Amet’s claim it is my understanding that the clinical picture in autism is heterogeneous. Common clinical characteristics have so far proved elusive. I remember David Amaral of the MIND Institute at UC Davis, speaking at the International Autism Conference held by the NAS in London 2005 showing a slide that said,

“Autism is an enormously heterogeneous disorder. It is likely to have a variety of etiologies and ultimately to be considered distinct variants or phenotypes of the same disorder (Autism type A, Autism type B etc.)

To date, research on autism has been too fragmentary to allow determination of the biomedical and behavioural characteristics that define different phenotypes of autism spectrum disorder.”(Amaral 2005)

Amet also claims that,

“The biomedical approach to autism is currently endorsed by over 500 medical doctors, throughout the world in a total of 23 countries. What these practitioners advocate is that autism is treatable. They uphold the principle that children with autism not only have the right, like any other children, to full medical investigation, but that the investigation must be comprehensive.”

Amet is wrong and she knows it. The five hundred medical doctors do not exist. She is referring to the DAN list of registered practitioners who have agreed to the DAN protocol for treating autism. Amet know that not all of these practitioners are medical doctors because she, a research scientist, is on the list. So is Ken Aitken, a psychologist and associate of Amet’s in the Autism Treatment Trust. Neither is qualified to call themselves an MD. The DAN list also includes naturopaths, homeopaths and other ‘alternative’ therapists.

Many of the DAN practitioners are medical doctors. But that is no guarantee of quality. Last year Abubakar Tariq Nadama died while being given chelation therapy. He was referred to Dr Kerry by DAN practitioner Dr Usman who recommended treatment with disodium EDTA with a dose of 50mg per kilo when the recommended dose is 40mg per kilo. Usman referred Abubakar to Kerry because “He apparently has a very high aluminum and has not been responding to other types of therapies and therefore she is recommending EDTA, which we do on a routine basis with adults.” Abubakar was five years old and autistic. His mother took him to America because she was persuaded that autism is treatable by the biomedical interventions championed by Amet.

At the time much was made of the fact that Kerry was not a DAN doctor. He is now. After he killed Abubakar, Kerry was admitted to a DAN conference, completed an eight hour intensive training programme and joined the “500 medical doctors, throughout the world” whom Amet looks to for endorsement.

Those “500 medical doctors, throughout the world” also include a Dr. Schwartz in California who is not allowed to examine boys without a chaperone because of previous misdemeanours. The Medical Board of California (2006) is currently trying to permanently revoke his licence to practise medicine after he persistently broke their injunction not to examine boys without a chaperone.

He chose to get round this problem by inventing a novel way to “uphold the principle that children with autism not only have the right, like any other children, to full medical investigation, but that the investigation must be comprehensive.” He interviews their mothers instead. And, without ever seeing the boys, orders a series of tests and prescribes treatments for them.

This is the company that Amet keeps. These are a few of the medical doctors who endorse her biomedical approach to autism. I am surprised that the NAS would publish an article that is so weak on logic, so riddled with factual errors and, above all, so ethically compromised. It is no more than a thinly veiled advertisement for her clinic, a commercial for autism treatments that are not supported by the literature rather than a serious discussion of that literature.

References

Amaral, D. (2005) A Multidisiciplinary Biomedical Approach to Autism Research: The Autism Phenome Project. Presentation to the NAS International Conference September 2005
http://www.nas.org.uk/content/1/c4/78/67/Friday_DavidAmaral6.pdf
(accessed 1/12/2006)

Amet, L. (2006)Biomedical interventions in autism. Communication 40:4 pp 10-11

Chakrabarti, S. Fombonne, E. (2001) Pervasive Developmental Disorders in Preschool Children. JAMA, June 27, 2001 – 285:24 pp 3093-3099

Chakrabarti, S. Fombonne, E. (2005) Pervasive Developmental Disorders in Preschool Children: Confirmation of High Prevalence Am J Psychiatry 2005; 162 pp 1133–1141

Ehlers, S. & Gillberg, C. (1993): The Epidemiology of Asperger syndrome. A total population study. Journal of Child Psychology and Psychiatry, 34:8 pp 1327-1350

Fombonne, E. (1997) Prevalence of autism spectrum disorder in the UK. Autism 1:2 pp 227-229

Kanner, L (1943) Autistic Disturbances of Affective Contact. Nervous Child 1943; 2: pp 217-250.

Medical Board of California (2006) Accusation and petition to revoke probation
http://publicdocs.medbd.ca.gov/pdl/Image.aspx
(accessed 1/12/2006)

NAS (1997) How many people have autistic spectrum disorders? NAS Factsheet
http://www.nas.org.uk/nas/jsp/polopoly.jsp?d=299&a=3527
(accessed 1/12/2006)

Science Blog (2004) Brain Inflammation found in autism.
http://scienceblog.com/community/older/2004/520044596shtml
(accessed 27/11/2006)

Wing L, Gould J. (1979)Severe impairments of social interaction and associated abnormalities in children: epidemiology and classification. J Autism Dev Disord. 1979: pp11-29