Thursday, August 31, 2006

My Turn at the Book Meme

I've been tagged by Abfh. Let's see...

One book that changed my life

I'd have to go with a book I don't have anymore and don't remember the title of. It was a BASIC programming manual of some kind I read and referenced many times when I was a young teenager. That was many years before Intel-based PCs became widely available. I remember distinctly that the BASIC software available in the 16K-RAM computer I played with at the time was made by Microsoft, though – likely coded by Bill Gates himself.

One book that you've read more than once

Hmm... I'm not sure I've ever done that.

One book you'd want on a desert island

Obviously, something such as "SAS Survival Handbook: How to Survive in the Wild, in Any Climate, on Land or at Sea".

One book that made you laugh

There are many. One that comes to mind is "Seinlanguage" by Jerry Seinfeld. It's basically a compilation of all his usual observational comedy, but it was a funny read.

One book that made you cry

Pass.

One book you wish you had written

I'll name several. "A Brief History of Time" by Stephen Hawking. "Cosmos" by Carl Sagan. And "The Selfish Gene" by Richard Dawkins.

One book you wish had never been written

I can think of at least a couple. I'll say "Evidence of Harm", not because it hurts a political stance, but because it's a waste of good paper and people's time.

One book you're currently reading

I'm in between books, but a couple weeks ago I finished reading two: "Through the Eyes of Aliens" by Jasmine O'Neill; and "Teaching At Home: A New Approach To Tutoring Children With Autism And Asperger Syndrome" by Olga Holland.

Jasmine O'Neill's book is great and I strongly recommend it. She's not afraid to explain why she experiences autism as a beautiful thing, despite her impairments. That's the kind of thing that should give pause to anyone who compares autism to cancer or AIDS. Jasmine also offers practical advise to parents.

Olga Holland's book is not bad, and offers practical advise, but she clearly does see autism as a disorder that must be defeated and autistic children as defective in some way. Traits of her child she perceives as negative are considered part of his autism; traits perceived as positive are not considered part of his autism. She uses a variation of the "social stories" teaching method throughout the book. In the end she tells how her son tests in the top percentile in some standardized test and enters a gifted program at school. (While being in the top percentile at something is statistically as abnormal as being in the lowest percentile, it is interesting that it is not perceived as such culturally). The author also spends much of her time discussing how horrible communism was in the Soviet Union – which I found to be irrelevant and uninteresting political commentary.

One book you've been meaning to read

"Thinking in Pictures" by Temple Grandin.

People to tag

I'm tagging Not Mercury, Dad of Cameron and Kevin Leitch.

Saturday, August 26, 2006

Why Biomed Will Always Have Little To Show For Itself

With all the hype about MeB12, DMSA, ALA, GFCF, multivitamins and so forth, you might think that there are good reasons to believe these biomed treatments are in some way effective. The reality is that there is not a single biomed treatment for autism that may be deemed clinically proven – not a single one.

And there are some historical embarrassments in the autism biomed field too. I already discussed Secretin, which Bernard Rimland had claimed to have a 75% improvement rate. This was before double-blind studies showed Secretin to be, at best, as effective as placebo. Don't be surprised if the exact same thing happens to DMSA, MeB12 and the others.

Some readers might be thinking that I'm forgetting Vitamin B6, an old but still popular biomed treatment, which does have some placebo-controlled studies under its belt, many of them showing positive results. But note that Nye & Brice (2005) conducted a detailed literature review and concluded that "due to the small number of studies, the methodological quality of studies, and small sample sizes, no recommendation can be advanced regarding the use of B6-Mg as a treatment for autism."

Multivitamins and supplements could arguably be of benefit to overall health, and thus appear to be effective in treating autism. That is how I interpret the results of Adams & Halloway for example. Readers will note that multivitamins in this study were effective in improving sleep difficulties and gastrointestinal symptoms, but had a non-significant effect (compared to placebo) on autistic features such as language, sociability and behavior. If these results are replicated, it would seem that it is a good idea to use multivitamins with children who have sleeping and gastrointestinal problems. This is probably even the case with non-autistic children.

So why is autism so resistant to biomed treatments? Autism biomed is based on a flawed hypothesis. It assumes that autistic children's brains are just about typical, except for a reversible biochemical imbalance or contamination of some kind. Biomed proponents often compare autism to being drunk or stoned. This, of course, is wishful thinking and fails to acknowledge much of what has been found about autistic neurology and cognition.

Autistic brains are different to neurotypical brains. Of course, some will be closer to neurotypical brains than others, but in general, it is known that autistic brains have a different distribution of grey and white matter, different neuron density, neuron size, different overall volume and so on. Autistic cognition is different to neurotypical cognition, with different strengths and weaknesses apparently. I contend that there is very little biomed treatments can do to compensate for these differences and force an autistic brain to work like a neurotypical brain.

The autism community should do better than engage in wishful thinking and waste all this time and resources with biomed. I suggest that autistic children should (1) be educated by engaging their strengths, (2) allowed to exercise their interests, (3) respected for the unique individuals they are, not defective medical puzzles to be solved, and (4) have their true (proven) medical issues, if any, addressed as medical issues, not as part of their very being, which is what autism is.

Friday, August 18, 2006

A Different Type Of Minority?

Abfh found an article titled Alone in autism – unfortunately including what has become a standard negative portrayal of autism, including the all-too-familiar scenario of a parent considering the murder/suicide of an autistic child.

Like Abfh's post, this post is not about the article either, but about the comments posted by readers. In particular, I think comments by Mary Grace are note-worthy. Mary Grace is a teenager diagnosed with Asperger's syndrome, who is herself featured in the article.

Mary Grace argued that autism can have "horrible disadvantages" and that this justifies a pro-cure position in regards to autism. She further stated that "there are probably dozens of stories where poor social skills have resulted in people being jailed or worse." When I try to discern the merit of an argument such as this, I prefer to think in analogies. So I mentioned that being black can entail "horrible disadvantages", particularly if we go back in history, and that being black has resulted in people being jailed or worse.

Mary Grace replied to my analogy as follows:

You don't have to do anything to be seen as black, it's just there. Social skills are different. They aren't always obvious as present or absent at first, and they can be improved upon. If a person with poor social skills (not necessarily AS, just poor in general) is arrested, aren't they more likely to show the worst of their traits and get themselves in more trouble? Social skills are important for anybody to have, and because of the nature of AS, we have to work extra hard. It's noit fair, but that doesn't change it. And I would like to emphasize that I most certainly do NOT buy into stigmatization of anyone for any reason, but I do acknowledge that stigmatization exists. And it does exist against people with poor social skills, and, as you said, against people of certain races. You can't change your race. But you can improve your social skills. That's where your arguement fails, I'm afraid. And it does suck to have poor social skills, or at least it sucked for me. I'm much happier now.


Essentially, Mary Grace argues that autistics are a different type of minority to blacks or gays or women or disabled minorities. If you are black, you can't do anything about that. If you are blind, there's not much you can do about it either in terms of regaining sight. But if you are autistic, and suffer due to your lack of social skills, you can work on improving your social skills.

Certainly, if you want to improve a skill, you can practice it. I'm a big believer in hard work and in that if you want to become better at something, you study it, and you practice, practice, practice. So what's wrong with this argument?

First of all, it is necessary to acknowledge that the world is full of physical limitations. I could practice basketball 10 hours a day for years and never become anywhere near as good as Michael Jordan. This is an example taken to the extreme, but it serves to illustrate that practice is not necessarily sufficient, and this applies even when trying to attain a "normal" level of skill. To presume that it is possible to achieve just about anything through hard work is wishful thinking. Optimism is a good thing, but unrealistic expectations are unhelpful.

Second, Mary Grace seems to suggest that autistic people have a responsibility to work hard on their social skills for their own good and for the common good. But is this the right thing to work for? Mary Grace says that black people cannot become less black, but I don't think this is even true. (Readers might be thinking of Michael Jackson at this point, but that's not what I mean). Couldn't black people "act white" so they can be more easily assimilated into white culture? Couldn't gays work hard at being attracted to the opposite sex? (There are behavioral interventions available). Should women who want to succeed in the work place act more like men in order to achieve their aims?

The deaf community has had to go through a similar debate, i.e. should deaf people be taught to sign and become part of deaf culture, or be taught oral methods (including lipreading) so that they can participate in the larger culture? My understanding is that deaf people, as a rule, favor manual methods. See Arguments in favor of Oralism are refuted by Manualists and Oral vs. Manual Debate.

Mary Grace also says she's happier now that she's learned social skills and is able to pass for normal. It's a good thing that she feels happy with herself and I don't want to imply otherwise. But it's also an experience contrary to that of other autistics, who say that when they stopped trying to fit in and started to accept what they were and no longer saw autism as a horrible thing, they became less depressed and anxious and so on.

Finally, while I disagree with Mary Grace, I just want to say that some of the responses she got, questioning her diagnosis, are out of line. This was debated already in Who can call themselves autistic? over at Ballastexistenz.

Saturday, August 12, 2006

No Autism Epidemic: An Update

This is a revision of a post I wrote about 5 months back. I will include many new arguments and data I've come across since then. As usual, those who believe that an autism epidemic has definitely occurred are invited and encouraged to debate the evidence presented.

Changing characteristics

Dr. Eric Fombonne has said that comparing current autism prevalence to a prevalence from studies 30 years ago is like comparing oranges to sheep. Another way to express this is that the diagnoses are not equivalent. But even with (presumably) the same subjective diagnostic criteria it is possible for diagnosed groups of autistics to be inequivalent as time goes by. This hypothesis (let's call it the expanding criteria hypothesis) is verified by looking at client characteristics in the California DDS data. See Table 1.


Table 1: Changes in autistic client characteristics over time
QuarterEpilepsyProfound MRSevere BehaviorsLack of MR
Q2 199215.6%11.2%22.9%27.8%
Q4 199611.8%7.4%20.5%41.2%
Q4 20008.7%4.4%19.2%52.4%
Q4 20047.1%2.6%17.4%61.9%
Q4 20056.7%2.4%16.8%63.6%


Every quarter, as caseload rises above what would be expected from changes in the population of the state of California, the proportion of certain characteristics of CDDS autistic clients simultaneously drop. As a group, autistics in California today are quite inequivalent to autistics in California in 1992. Effectively, autism one quarter in California is not equivalent to autism the next quarter. Therefore, it is not possible to say that a real increase in autism prevalence has occurred.

The following figure [courtesy of CDDS] also illustrates the point. Notice that the autism curve and the autism without MR curve run almost parallel to one another.



Evidence from regional differences

The bulk of the "epidemic" in the state of California occurred in the Los Angeles area, as illustrated by the following figure [courtesy of CDDS]:



Current differences in administrative prevalence between regional centers are substantial. Table 2 shows caseloads of various CDDS categories in the Westside RC and the Central Valley RC, expressed as ratios to the epilepsy caseload.

Table 2: Q4 2005 comparison of Westside and Central Valley
Regional CenterAutism RatioPMR+SMR RatioPMR RatioEpilepsy RatioSevere Behavior Ratio
Central Valley0.320.600.361.00.31
Westside1.610.680.311.00.45


It is telling that despite the 500% difference in administrative prevalence of autism between Westside and Central Valley, there is apparently no difference in the prevalence of mental retardation between these two regional centers. If regional prevalence differences are not real, we can extrapolate and conclude that state-wide prevalence changes over time could also not be real.

The hypothesis that regional prevalence differences may be due to environmental factors, such as pollution, appears to be improbable, as I recently argued.

Caseload growth patterns are telling in that regard. Note that the highest annual caseload growth (in percentage terms) in California occurred in the 2002-2003 timeframe. It was about 20%. Currently, the Central Valley regional center, which has the lowest prevalence of autism in the state, has an annual caseload growth of 24%. Autism in Central Valley is currently undergoing what might be described as staggering growth. In contrast, the Westside regional center, with the highest prevalence in the state, has an annual caseload growth of just over 8%. It is not far fetched to suppose that, eventually, Central Valley will catch up to Westside, and that it was simply behind in its recognition of autism.

Evidence of diagnostic substitution

Shattuck (2006) found that as the prevalence of autism has risen in the United States, the prevalence of idiopathic mental retardation and learning disability has undergone a corresponding decline.

California was one of a handful of states that does not clearly follow this pattern, according to Shattuck. But as noted, expanding criteria is what apparently drives most of the autism caseload growth in California. We also know that the recognition of autism in the population with mental retardation in California was around 3.5% in 1992, whereas it is about 7% today. This recognition varies considerably from one regional center to the next. Typically, but not always, regional centers with lower autism prevalence have a lower proportion of clients with autism in the mental retardation category. Note that de Bildt et al (2005) states that the most reliable and well-founded estimate for the prevalence of PDD in children and adolescents with mental retardation is the DSM-IV-TR prevalence of 16.7%. So the California recognition of autism in this population still has considerable room for additional growth, and it is not far fetched to conclude that improving recognition (i.e. diagnostic substitution) has occurred in California over time, even though this is not the most significant factor driving caseload growth in that state.

High prevalence in adults

Stahlberg et al (2004) found that 30% of consecutively referred adult patients with ADHD had "comorbid" ASD. If we consider that the prevalence of ADHD in adults is estimated at about 4.2% as of 2006, it would appear that the prevalence of ASD in adults can be at least 126 in 10,000. Granted, Stahlberg's ADHD patients could be more "severe" than usual, but his findings are notable considering the limited screening of a specific population.

Nylander & Gillberg (2001) found that 89.5% of adult psychiatric outpatients with "definite ASD" had previously been missed. They had received other psychiatric diagnoses, such as schizophrenia.

Baron-Cohen et al (2001) found that 2% of randomly selected adult controls scored 32 or higher in the AQ test. Further, 7 of 11 interviewed students who were high-scorers met threshold criteria for a DSM-IV diagnosis. It would appear then that the prevalence of ASD in adults can be as high as 127 in 10,000 if screened thoroughly. This does not even consider those autistics who are missed by an AQ score threshold of 32.

Mark Blaxill's "hidden horde" appears to not be hiding very well, because it has been found repeatedly.

Evidence from prevalence studies

Mike Stanton has posted a detailed analysis of autism prevalence studies as part of a rebuttal of Richard Lathe's book "Autism, Brain and Environment".

When we compare apples with apples, the huge increases of autism prevalence often claimed to have occurred seem to vanish. Williams et al. (2005) provides a systematic review of prevalence studies. The researchers conclude that 61% of the variation among prevalence studies may be explained by a model that includes diagnostic criteria used, age of children screened, and study location. Note that this model does not even consider awareness or cultural factors.

What went on in the past

Lorna Wing was there and explains it well:

One of us (LW) was involved in the planning of the study by Vic Lotter [1966] of 78,000 children aged 8, 9, and 10 years living in the former English county of Middlesex. This was the study in which the 4-5 in 10,000 prevalence rate was first found. I (LW) know what sorts of children were included as classically autistic because I was one of the small group (Neil O'Connor, John Wing, Vic Lotter and myself) who decided on the criteria. In those days we were interested only in really classic Kanner's syndrome and Vic was determined to keep the criteria as narrow as possible. Later, in the Camberwell study described above, Vic was shown case histories of the children Judy Gould and I thought fitted Kanner's descriptions - to our surprise, Vic said we ought to exclude some because they were not classic enough! I think it is fair to say that, when Vic specified narrow criteria, they were NARROW.

When Judy Gould and I started the Camberwell study, we still thought that Kanner's autism could easily be differentiated from other developmental disorders.. By the end of the study our ideas had been turned upside down. We had learnt from direct experience that the psychological dysfunctions underlying autism were manifested in many different ways, far beyond the boundaries of Kanner's syndrome. We developed the hypothesis of an autistic spectrum based on the triad of impairments of social interaction, communication and imagination. Because we concentrated on the children with learning disabilities (IQ under 70) we saw very few with the pattern described by Asperger. We had to wait for the study by Christopher Gillberg in Gothenberg to find out how many children with IQ of 70 and above were also in the autistic spectrum. As described above, combining the results of these two studies gave an overall prevalence rate for the whole autistic spectrum, including those with the most subtle manifestations, of 91 per 10,000 - nearly 1% of the general population.


The epilepsy argument

Autism has been linked to a seizure liability, and the CDDS data itself shows that the prevalence of epilepsy among autistics is considerably higher to that of the general population. It follows that an environmental trigger capable of producing an epidemic of autism might also result in an epidemic of epilepsy. Surprisingly, we find in the data that the epilepsy caseload grows at about the same pace as the population in the state of California. Additionally, the prevalence of epilepsy does not appear to depend on degree of urbanization.

The mental retardation argument

An epidemic-causing environmental trigger that results in brain injury should be expected to increase the probability that an individual will have mental retardation, and thus result in an epidemic of all levels of mental retardation. But again, there is no evidence of an increase in the prevalence of mental retardation. In California, the mental retardation caseload increases at about the rate that should be expected from population growth.

Furthermore, it is known that the average IQ score has actually risen over time and IQ tests have to be re-normalized periodically (see Flyyn effect). While this does not necessarily say anything about autism, it should at least put to rest fears that an epidemic of neurological disorders will "destroy the United States."

The institutionalization argument

Proponents of an autism epidemic generally not only refer to autism, but to an increase in the prevalence of all sorts of neurological disorders. They also often refer to the increased fiscal burden that will presumably result from this epidemic. While increased awareness can result in increased service expenses, I contend that there are certain types of services that are not likely to be significantly affected by increased awareness. Let's look at institutionalization of developmentally disabled individuals in the state of California.

In Q2 1992, the total number of institutionalized individuals registered with CDDS was 32,943. In Q2 2005, the number was 36,869. Adjusting for population growth, we get 10.6 per 10,000 persons institutionalized in 1992 vs. 9.97 per 10,000 in 2005. There appears to be a decrease in the prevalence of institutionalized individuals with developmental disabilities, which is a positive trend.

Granted, very young children would not tend to be institutionalized, but even in the younger age cohorts the CDDS data shows a decreasing trend in number of institutionalized clients. At the very least, this should lay to rest fears that a generation from now institutions will be overflowing with adult autistics.

The speech delay argument

Speech delay is perhaps the most characteristic feature of autism. If there has truly been an epidemic of autism resulting from an environmental trigger which is not necessarily autism specific, one might expect to find an increase in the prevalence of speech delay. There is no evidence of such an increase. Epidemiological data is hard to compare due to differences in methodology and criteria, but let's look at some studies over time. Stevenson & Richman (1976) found a prevalence of 3.1% for delayed language development and 5-7% for specific language delay. Silva et al (1987) reported a prevalence of 4.6% for expressive language delay. Wong et al (1992) found a prevalence of 6.1% for expressive language delay. Shriberg et al (1999) found that he prevalence of speech delay in 6-year-old children was 3.8%. There are no indications of an increase in the prevalence of speech delay concurrent with the "autism epidemic".

Refutation of a common argument

A study by the MIND Institute (2002) determined that there was "no evidence that a loosening in the diagnostic criteria has contributed to the increased number of autism clients served by the Regional Centers." These findings have often been cited in favor of the epidemic argument. The study assesed an earlier cohort and a more recent cohort of clients using the DSM-IV criteria. Since both cohorts met the criteria at the same rate, the researchers concluded that a losening of the criteria cannot account for an increase in autism prevalence. Gernsbacher et al document the obvious reasoning flaw, using a height analogy. Briefly, while both cohorts meet DSM-IV criteria, they are not necessarily equivalent. It is possible the earlier cohort meets a more restrictive criteria than DSM-IV which the more recent cohort might not.

Conclusion

The state of the evidence is not simply sufficient to allow suspending the belief that an epidemic of autism has occurred. It is my opinion that there is enough evidence to assert that said epidemic did not occur.