Tuesday, November 24, 2009

A Word About Hertz-Picciotto & Delwiche (2009)

The recent Chicago Tribune Articles have resulted in a flurry of reactions, particularly from AoA. I'd like to discuss just one of them in this post. Kent Heckenlively was complaining that the Chicago Tribune reporters did not give weight to any of the documentation he had provided them. Specifically, to support the assertion that we are in the midst of an autism epidemic, Heckenlively cited a press release by the MIND Institute.

Why cite the press release and not the paper? Well, that's because the conclusions of the paper said the following.

Other artifacts have yet to be quantified, and as a result, the extent to which the continued rise represents a true increase in the occurrence of autism remains unclear.


A true increase... remains unclear. Is that clear enough?

The paper is titled "The rise in autism and the role of age at diagnosis." I'll refer to it as Hertz-Picciotto & Delwiche (2009). I've already criticized multiple aspects of the paper (last time here) but I'd like to say a few more things about it.

The conclusions of the paper seem refreshingly honest, but I'm guessing they are that way simply to get through peer-review. The missing artifacts are not just any artifacts, either. One of the artifacts that did not enter the calculations is key: awareness. It would be nonsensical to assume that awareness of autism has not changed since the early 1990s.

But what did the press release say?
“It’s time to start looking for the environmental culprits responsible for the remarkable increase in the rate of autism in California,” said UC Davis M.I.N.D. Institute researcher Irva Hertz-Picciotto, a professor of environmental and occupational health and epidemiology, and an internationally respected autism researcher.

Hertz-Picciotto said that many researchers, state officials and advocacy organizations have viewed the rise in autism's incidence in California with skepticism.

(source)

This is completely at odds with the conclusions of the paper, and I find it quite dishonest. To make it perfectly clear, yes, I'm accusing Dr. Hertz-Picciotto of intellectual dishonesty.

Dr. H-P further states that:
“These are fairly small percentages compared to the size of the increase that we’ve seen in the state,” Hertz-Picciotto said.

Is that even true? The paper finds that a 2.2-fold increase may be explained by changes in diagnostic criteria, 1.56-fold due to inclusion of "milder" cases, and 1.24-fold due to changes in age at diagnosis. If you multiply these factors, you come up with a 4.26-fold increase that may be explained by just these 3 artifacts.

That's 62% of the entire rise the authors were attempting to explain. Maybe 62% is a "fairly small percentage." In this case I'm going to give Dr. H-P the benefit of the doubt and say that she likely didn't know the factors needed to be multiplied. There are no indications in the paper that a calculation of the overall contribution of the 3 artifacts combined was even attempted. I won't even get into statistical uncertainty.

The flaws of the analysis are not what bother me the most, however. Consider this. What is the value of this study? Why was it carried out? If you're trying to determine whether artifacts can explain the rise in autism service classifications in California, and you cannot estimate the contribution of all relevant artifacts, what is the point of the analysis?

Here's an analogy. Suppose you wanted to determine if global warming can be explained by the greenhouse effect. In order to do this, you estimate the contribution of methane, water vapor and nitrous oxide to recent temperature increases, but you leave out CO2. You conclude that those 3 gases alone cannot explain the entire rise in temperatures, but perhaps that's because you did not consider the biggest contributor to the greenhouse effect: CO2. Then you tell the media that greenhouse gases cannot fully explain the rise in temperatures.

Wouldn't such a study be better understood as a propaganda effort, rather than a contribution to scientific knowledge?

Someone might complain that Hertz-Picciotto & Delwiche (2009) does contribute to scientific knowledge, because it tells us about the impact of certain artifacts. But does it actually do that?

Take what is perhaps the most important artifact the paper does take into account: changes in diagnostic criteria. What would you do if you wanted to determine the impact of changes in criteria? You might carry out a prevalence study with good case-finding that uses two different criteria on the same population: DSM-IV and DSM-III (or perhaps Kanner criteria.) Hertz-Picciotto & Delwiche (2009) does not do anything that even resembles this. They use data from a separate study, so they didn't even contribute new data. We can't even be sure how well the data from Finland might apply to California. The case-finding of the Finnish study is not necessarily very good either. Plus it's just one data point, with all the uncertainties implied by that.

To determine the impact of inclusion of "milder" cases (i.e. anything that is not "autistic disoder"), what would you do? I think you could evaluate a random sample of CalDDS autistic children and diagnose them with either autistic disorder, PDD-NOS or Asperger's. What the researchers did instead was use data from a separate MIND Institute study where CalDDS children had been evaluated with the Autism Diagnostic Observation Schedule (ADOS) and the Autism Diagnostic Inventory (ADI.) Are these diagnostic tools even able to accurately distinguish between autism spectrum diagnoses? I'm not aware of any evidence that they do.

In other words, the MIND Institute study is not even informative about the impact of the artifacts it did take into account. I frankly can't see this study as a contribution to scientific knowledge at all. It gives the appearance of being part of a propaganda effort.

Monday, November 23, 2009

Chicago Tribune Articles

I'm just going to link to the Chicago Tribune Articles below.

What do readers think?

You can probably tell I "stole" those links from Orac. I'll also link to his post:

I noticed that "biomed" pushers have shown up in comments, and their primary counter-attack seems to be roughly this: "FDA-approved drugs also have serious side-effects!"

They do. Anti-psychotics, especially, can have nasty albeit rare side effects like neuroleptic malignant syndrome. But the biomed people are just trying to change the subject, aren't they?

Feel free to use the comments section to discuss the ethics of FDA-approved drugs for autism. Do the benefits documented in trials outweigh their more serious side-effects? Are there concerns about the evidence of their efficacy? Do we even understand how they work?

Tuesday, November 10, 2009

False Despair

What would be the value of telling a parent of a recently diagnosed autistic child that the child will never be able to hold a job, if this is unlikely to be true for a good majority of autistic children diagnosed at present? Is there any? I just don't see it. In fact, I think this would be at least as harmful as telling a parent that their child will grow up to be just like Dr. Temple Grandin.

I was recently told that I shouldn't divulge data that could be interpreted as painting a "rosy picture" of autism. It's not only rude to tell people what they should or shouldn't write about, but this kind of suggestion is quite unreasonable in my view.

Beyond the merits of the idea that it's best to presume competence, I believe one should have realistic expectations based on actual data, rather than vague assumptions based on stereotypes and outdated information of unclear origin.

I also think it's highly questionable to dismiss new findings solely on the basis that they "don't feel right" or because they fail to confirm one's preconceptions and personal experience. This is the very definition of closed-mindedness. (A lot of people seem to think "closed-mindedness" means you are not willing to accept pseudo-scientific claims, but this is simply not true.)

It's important that data is current too. It would be completely dishonest to pretend that autistic children diagnosed today are just like the children who were called autistic in, say, the 1960s. That's simply not a realistic view. I have discussed adult outcome studies in the past, and I think they are relevant, but they need to be understood in their proper context. For example, 61% of autistics born in 1983-1985 receiving services under the autism category in California were identified as having intellectual impairments. Meanwhile, only 27% of those born in 1993-1995 are identified the same say (Gernsbacher et al. 2005; The MIND Institute 2002.) This is despite the fact that California DDS has eligibility restrictions, sometimes interpreted to mean that only persons with "full syndrome" autism are eligible (which is probably an untrue assumption, but it's also the case that not all persons with an ASD diagnosis are necessarily eligible.)

I say this knowing full well that my own son is different to most autistic children diagnosed today, and perhaps more like children who were called autistic in the 1960s. I expect my readers to be similarly capable of distinguishing personal realities from population-level realities. If I divulge data applicable to autistics who don't have intellectual disability, and you have an autistic child with intellectual disability, then the data does not apply to your situation. I think this should go without saying.

If you look at really good paper critiques, you will find a common characteristic: They don't just point out limitations and errors; they explain how the limitations and errors could make the results what they are, in the event that the hypothesis the authors have advanced is incorrect. This typically involves pointing out details the authors have apparently overlooked. For examples of remarkably good paper critiques, see the Photon in the Darkness Blog.

Then you have really poor paper critiques. These come in various flavors. Perhaps the lowest form of critique is the ad hominem circumstantial, otherwise known as an appeal to motive: "I suspect the author is biased, therefore the results of the paper are probably wrong." This is essentially a useless critique, since all authors of all papers could be suspected of having a bias. Some additional criteria is required to make it worthwhile. For example, if a researcher is known to have engaged in substantial scientific misconduct (e.g. plagiarism), then it is reasonable to hold all subsequent works by the same author to be suspect a priori. It would also help to explain how the bias might alter the results. In a hypothetical case, it could be reasonable to speculate along these lines: "Since the study was not blinded, it's probable that researcher bias could have inadvertently altered the results of the assessments." This is a plausible explanation, as opposed to a simplistic insinuation.

Another precarious form of critique is what I'll call the critique by anecdote or personal experience. Example # 1: "How could this global warming theory be true? It was really cold this winter." Example # 2: "I have never seen any autistic adults, and I know 'em when I see 'em, so this really expensive and exhaustive prevalence study just cannot be right."

BTW, how is it that David Kirby knows 'em when he sees 'em, if he's never seen them at all?

There are some reasonable forms of critique that don't require much effort. Appealing to the unreplicated status of a result is one example. This is a good convention that is part of the scientific method. "The result could be of interest, but let's reserve judgment until it's replicated."

Some people have said they don't yet buy the prevalence result from the NHS study because the study is unreplicated. In this particular case, I believe they are mistaken. For one, there's considerable prior evidence that autism can be found in various populations of adults where previously it was largely unrecognized. Furthermore, Kadesjö et al (1999) found a prevalence of 1.21% among children born in 1985 in the small town of Karlstad, Sweden. The "children" happen to be 24 now. If the study were done today, on the same exact cohort, it would be considered an adult prevalence study. In this sense, the NHS study may be considered a replication.

Let me make this clear. There's simply no excuse to continue to claim that autistic adults are a non-significant population compared to the population of autistic children. Doing so is just another form of denialism.

Wednesday, November 04, 2009

Jonathan's Completely Dishonest Attack on My Latest Posts

Dear reader: Please go read Jon Mitchell's utterly dishonest attack on my two latest posts. It's titled Some neurodiversity potpurri.

First of all, I'd like to inform Jon that even though I've said this blog is pro-neurodiversity, I'm not a leader of neurodiversity proponents or anything of the sort. All my opinions are personal and should in no way be seen as opinions put forth by something called neurodiversity. It's very uncool to try to use what I say (or what other bloggers say for that matter) as a way to attack the neurodiversity philosophy as a whole.

Now, the most outrageous misrepresentation of what I said is the following:
I see that Joseph of the autism natural variation blog has decided based on one published report based on the statuses of only 19 people that adults with autism don't have problems with employment nor with marriage.

I could've predicted this was going to be Jon's response, and it's not the first time he's tried to misrepresent what I've said. I'll leave statistics for the end of the post. I want to discuss the misrepresentations first.

What I said about lack of employment is that (1) figures used in prior estimates appear to be exaggerated; (2) that it would seem adult autistics who live in private households across the UK are largely productive individuals who contribute to the economy in a manner similar to their non-autistic peers.

I never said autistic people don't have problems with employment. All I said is that autistics are largely employed. There's a big difference. The data can't tell me anything about specific problems autistic people have with employment, and I have no doubt there are a variety of problems.

I stated that there appear to be some differences in the employment rates of autistics and non-autistics, but the authors didn't find them statistically significant. This is what the authors said:
No significant variation in rate of ASD by economic activity status was found.

That's a true statement. If you want to lash out at the authors for daring to say that, be my guest.

The misrepresentation of my claims about marriage is even more outrageous, since my post clearly said in bold that autistic people in the UK are apparently about half as likely to get married than non-autistic people.
In the past Joseph presented some statistic saying that 25% of autistics were employed. As far as I can tell he neglects to mention any source or reference or link for this statistic in any post on his blog.

OK, that one is my fault. I failed to cite a reference in the old post, and I don't even remember the exact reference. I'm usually careful about that sort of thing. If you're interested, Howlin et al. (2004) reports that almost one third of the adult autistics in that study had some form of employment. Szatmari et al. (1989), a follow-up of adults without intellectual disability, reports a rate of employment of 50%.
So Joseph seems to imply that autistic persons are making just as much money as an NT.

I never talked about salaries, and if you made inferences from my post in regards to salaries, that's really not my fault. The study does have data on salaries. The summary of the findings was the following.
While the likelihood of having ASD appeared to increase among men as household income decreased, this was not significant (when analysis was run using household income
grouped into tertiles).

In this case, again, there might have been some differences, and if you look at the numbers in Table 2.3 it would be difficult to deny that autistics are making somewhat less money than non-autistics. But in a statistical sense, the numbers cannot tell us for sure that there's a difference.
So again, we have ND trivialization of an autistics inability to get married or make a living.

To Jon Mitchell, any figures and facts that don't agree with his personal views and experiences with autism constitute "trivialization." Reality doesn't exactly matter if it doesn't jive with what he sees as the necessity of continuing to have a grim worldview.

The Stats

Jon doesn't like the stats of the study because:
The authors of the reports extrapolated this number 19 to the greater population claiming that 1% of adults in the UK in private households have autism. However this was just a guess based on mathematical projections.

For starters, saying that the result is a "guess" is clearly an inaccurate characterization, and I've explained this previously. Many of the 19 autistic people identified must have been assigned a probability of selection that is less than 1.0 in phase 1. For example, if 10 of the 19 autistic people had been assigned a probability of 0.25, then clearly there must have been about 40 autistic people in the original group who were assigned a probability of 0.25. This is a probabilistically sound projection, not a "guess." (It's a bit more complicated than I explained, because there's also some weighing due to participation refusal based on some household variables.)

Now, no study can prove a negative, i.e. that there's absolutely no difference between the characteristics of two groups (this is the "null hypothesis.") All you can say is that you found the null hypothesis cannot be rejected. Of course, some studies are better able to rule out small differences as opposed to big differences, with statistical confidence.

It does matter that only 19 autistic people were found, but what mostly matters is the overall sample size. In Table 3.6 they indicate the confidence interval for ASD prevalence is 0.5% to 2.0%. They list the sample size as 2854 and the "weighed" sample size as 7358.

There are prevalence studies smaller than this, and existing data on the characteristics of autistic adults are usually based on comparable or smaller samples of autistic people.

The confidence interval is actually what you would get if you had found 7 autistic people out of 700 in a standard sampling (and I have some thoughts about implications of this, but I won't go into them here.)

Prevalence of ASD among adults who are employed was 0.9%. The confidence interval would be roughly equivalent to what you'd get if you had found 5 autistics out of 555 people, or 0.4% to 2.1%. (About 75% of all adults are employed in the UK.)

So on the one hand you have a prevalence of [0.5% - 2.0%] and on the other hand you have a prevalence of [0.4% - 2.1%]. Is there a difference? We just can't say there is.

Monday, November 02, 2009

Marriage Among Autistics, Or Why the NHS Study Obliterates CADD

In the previous post I discussed data that contradicts the common belief that autistic adults are largely unemployed.

In this post I want to discuss marriage. Marriage, again, is something that is considered very rare among autistics. It's a stereotype like any other stereotype, of course, but it's not an entirely unjustified one.

Of all the autistics Leo Kanner wrote about, I believe only one (Robert F) is known to have married. Said Kanner:
The contacts thus established led to the discovery that the boy-meets-girl issue was paramount in the talks of the companions. Again, there was a vaguely felt obligation to "conform." Those attempts were sporadic and short-lived. The "explanations" offered indicated that there was not too much displeasure with the absence of any real involvement.

Henry C. reported that he was single, that several girls "had hoped to change that" but that he had "no desire to get tied down for a good long time." Thomas G. declared categorically that girls "cost too much money." Clarence B., who "socialized" with a girl for a short time in college, stated that he "ought to get married but can't waste money on a girl who is not serious." Bernard S. was said to have approached a girl once for a date "in a very negative way" (inviting rebuff). Fred G. "experimented" once with a double date arrangement (never repeated).

George W. made things easy for himself by deciding a priori that girls were not interested in him. Sally S., the only girl in our group, once asked seriously at 23 years of age what she ought to do if ever she fell in love with someone, an experience she had never had before. She said: "I have never had the interest in boys most girls my age have." At 30 years, she dated a man for a few months but gave this up because she was "frightened by any intimacy."

(Kanner et al. 1972)

In several outcome studies we see the same pattern. Of the 16 autistic adults without intellectual disability from Szatmari et al. (1989), only one was married, even though 4 were dating regularly. Average age at follow-up was 26.1. From a recent outcome study out of Utah involving 41 autistic adults, we learn that only "a few" were married.

One problem with these findings is that adults in outcome studies are young adults. Additionally, we should not assume that diagnosed autistic adults, first identified when they were children, are representative of all autistics from the general population, known and unknown. Current understanding of autism is different to what it was in the past.

Once again, the NHS adult prevalence study proves useful in addressing these sorts of limitations in available data. The report tells us that the prevalence of ASD in three marital status groups is as follows.
Married/cohabitating: 0.5%
Single: 2.5%
Widowed/divorced/separated: 0.6%

There's also information on a "base" population that is not exactly representative of the general population, but it's probably close enough to being representative that it can be used to come up with estimated proportions of autistics and non-autistics in each of the categories.


Married/CohabitatingSingleWidowed/divorced/separated
Autistics33%57%10%
Non-Autistics61%22%15%


Data for men only:


Married/CohabitatingSingleWidowed/divorced/separated
Autistic Men30%63%7%
Non-Autistic Men61%26%14%


There are some differences. Autistic people in the UK are apparently about half as likely to get married than non-autistic people. I would not say the characteristic is diagnostic, however.

I should point out once more that the study only looked for autistic adults who live in private households. The data will likely change somewhat when autistics who live in "communal establishments" are considered.

Implications For CADD

I've previously criticized the concept of Cassandra Affective Deprivation Disorder (CADD). It's a pseudo-scientific, made-up and damaging idea to the effect that autistic people make for terrible significant-others and spouses to such an extent that they can cause their partners to develop psychological problems and health issues, even cancer.

If CADD had an ounce of truth to it, you'd expect divorce to be rampant among autistics. Heck, you'd expect autistics to widow more often, if the claim about effects on health were true.

Yet, the divoced-to-married ratio for autistics is 0.29, whereas the same ratio is 0.24 for non-autistics. (It's 0.24 vs. 0.22 for men only.) That's a minor difference, not significant by any stretch of the imagination.

It's clear that the reason a lot of autistic people in the UK are single is not because they fail at relationships. It's because they are not good at starting relationships.

The claim that autistic marriages fail much more often than expected is mythical, evidently. Nevertheless, many web pages state the following: "Dutch research suggests that the divorce rate for people with Asperger syndrome is around 80 per cent." Interestingly, this exact phrasing appears throughout the web, as if it had been copy-pasted. I have tried to locate the original source of the claim, to no avail. One person says they "lost the link."

The claim appears in a book by Ashley Stanford for people whose significant-other has Asperger's: "Preliminary research performed in Holland suggests that the divorce rate for couples in which one partner has AS may be as high as 80 percent (Relate leaflet)."

The Relate leaflet in question appears to be this webpage by none other than FAAAS. FAAAS, for those who don't know, is an organization of people who moan about their "frustrations" with their adult autistic relatives. FAAAS, not surprisingly, is connected to Maxine Aston of CADD infamy.

The claim that appears in the Relate leaflet is exactly the following:
For the partner of a person with AS, their bewilderment at the puzzling behaviour of their spouse can cause deep distress and a breakdown in their health. Inevitably this means that there is a high divorce rate amongst marriages where one partner has AS. Research in Holland suggests that this is as high as 80%, and research recently done in the UK is due to be published next year.

It's entirely unsourced. I'm currently skeptical as the the existence of the famous Dutch research.

Tuesday, October 27, 2009

Unemployment Among Adult Autistics in the UK

I've previously criticized estimates of the "costs of autism" to society. The whole rationale of coming up with such estimates is objectionable to begin with, but I've also criticized what appear to be exaggerations in the figures that form the basis of these analyses.

One key component of such estimates is "lost productivity" due to lack of employment and related metrics. I've pointed out that old data on the employment rate of adult autistics no longer applies. If you want to come up with cost estimates based on an ASD prevalence of 0.6% or 1%, you have to know the employment rate that corresponds to the ASD criteria that results in said prevalence. You can't just look at diagnosed adult autistics, and hope they are representative of all adult autistics, especially considering autism has been very much under-recognized in the past.

Of course, data that addresses this objection was not available until recently. That did not stop me from coming up with a guesstimate, though. I suggested that perhaps 70% of autistic children diagnosed today might end up being employable a generation from now.

I think it was clear in the blog post that this was a rough estimate extrapolated from other trends. The estimate, predictably, was met with accusations that I trivialize the challenges of autistics and so forth, specifically from Jon Mitchell. It seems that whenever I do some math or look up figures in the literature, I'm automatically engaging in trivialization.

Jon was of course "mystified" as to how I came up with the 70% figure, and implied that it's unbelievably high. Whenever he wants to snipe at me, this is the one thing Jon likes to bring up. He also proclaims I'm "one of the more prominent ND bloggers" so he gets to criticize not just me, but he probably thinks he's criticizing the entire neurodiversity movement in the process.

Readers are probably aware by now that the UK National Health Service recently released its first report on a prevalence study of autism in adults living in private households. The report includes some data on employment, but all the report says about it is this:
No significant variation in rate of ASD by economic activity status was found.

That's interesting enough by itself, but let's look at data from Table 2.4. There are 3 groups of persons considered in the study: Those in employment, those who are unemployed, and those who are economically inactive. The following is the prevalence of ASD in each group:

In employment: 0.9%
Unemployed: 1.6%
Economically inactive: 1.5%


The report also gives a "base" population, which consists of all persons from phase 1 who had been assigned a near-zero probability of ASD. You may recall that 7461 respondents were interviewed in phase 1. The base population consists of only 5998 persons, divided as follows:

In employment: 4492
Unemployed: 291
Economically inactive: 1215


The base population is not exactly representative of the general population (it's more "non-autistic" than normal if you will) but it will have to do. I will use it to estimate rates of employment and unemployment in autistics and non-autistics, as shown in the following table.

In EmploymentUnemployedEconomically Inactive
Autistics64%7%29%
Non-Autistics75%5%20%

There are some differences, but the study authors didn't find them to be statistically significant. In any case, it would seem that adult autistics who live in private households across the UK are largely productive individuals who contribute to the economy in a manner similar to their non-autistic peers.

Of course, this particular report doesn't tell us about autistics who live in "communal establishments." I've suggested that when all is said and done, pooled prevalence of ASD might turn out to be around 1.3%. Even if all autistics who live in communal establishments are considered unemployed, total unemployment among autistics might be around 35%.

Thursday, October 08, 2009

Is It More Like 1.2% to 1.5%?

Over two years ago I wrote a post titled Moving Toward a New Consensus Prevalence of 1% or Higher. At the time the prevalence of ASD was generally considered to be 0.6%. If you Google it, you'll find this figure is still the one that's cited most frequently. At present, no one has come out and precisely said the consensus prevalence has been revised to 1%, but I think that's pretty much where we're at. Consider what Roy Richard Grinker said recently to Time Magazine.
"It provides what scientists call convergent validity: no matter how you shake the bushes, you come up with this 1%," says Richard Roy Grinker, an autism researcher at George Washington University who has worked to determine ASD prevalence in South Korea.
(source)

Two years ago, and even long before this – as suggested by Lorna Wing – there were already some indications in the literature that 1% might be a more accurate figure. It was not a lucky guess or anything like that. My concern, which came to pass, was that as study methodologies evolved and awareness improved, the public would be frightened by what might appear to be a real increase in the prevalence of autism, with no end in sight. Ms. Clark (you remember her, right?) speculated that the process might be very gradual, with people getting increasingly surprised, and finally collapsing from exhaustion. It turned out to be a little more quick and relatively painless, at least so far.

I believe the question at this point is whether we've reached a plateau. Is prevalence going to stabilize at 1%? Have identification methods been pushed to their limits? Is the level of awareness (important in phone surveys and passive systems) the highest it's ever going to be?

I think that's possible, provided the same criteria and diagnostic tools continue to be used. But I gotta tell you, I have some reasons to believe we haven't seen the end of this just yet – not very many reasons, admittedly, but some. We might find that a more accurate number for prevalence is a little bit higher, perhaps 1.2%, or even 1.5%.

I'm not going to discuss cultural trends or the inherent subjectivity of psychiatric diagnoses, simply because this would be difficult, if not impossible, to quantify. But I do want to discuss case finding in this post.

What brings this about is the recent NHS prevalence study of autism among UK adults. The study has already been discussed by Anthony Cox, Kev Leitch, Sullivan, Catherina, and others. It found that 1% of adults living in private households had ASD. This result should come as no surprise to regular readers of this blog, particularly those who have read High Prevalence of Autism in Adults.

The NHS study did not look for autistic adults living in "communal establishments" (institutions.) According to the NAS, the report is "the first part of a much more detailed research project" (source) so I have little doubt there will be a follow-up that looks for adults in institutions. What will happen then? The NHS report says that 2% of all adults live in communal establishments. I believe pooled prevalence from both studies might turn out to be around 1.3%. It will easily be 1.2%.

Of course, there's some room for statistical uncertainty in these figures, and we'll have to wait for replications that use roughly the same methodology to see how the figures converge. But taking them at face value, 1.2% or 1.3% are a little higher than might be expected. Shouldn't the prevalence among children in the UK be even higher than this? Presumably, diagnostic stability to adulthood is not 100%, and autistics might have a slightly lower life expectancy than normal.

It's important to understand that the NHS study is not only the first of its kind, but also one with a methodology that is both novel and innovative. The methodology is designed so that the prevalence of ASD can be estimated even if the screening tools available to the researchers are unreliable and not well researched. The method does not require knowing how a screening tool performs a priori. It's preferable that the tools perform well – it helps with statistical power – but this is not a requirement per se.

I realize most people can't seem to make heads or tails of the methodology of the NHS study. I've tried to explain it with examples (e.g. here). You have my assurance that it's probabilistically sound. This can be proven mathematically.

That's not to say the methodology doesn't have any problems. Like any new methodology, it will be scrutinized in the scientific literature. Potential issues will be identified. Guidelines on how the selection probabilities should be defined will be proposed, etc. This is generally acknowledged by the authors:
The present methods are therefore felt by the authors to be to the highest standard achievable at present. However this is a first methodological development of its kind in the autism field and it is to be hoped that future surveys could build and improve on the present procedures.

Don't be surprised, though, if this methodology becomes a sort of standard that is subsequently used in studies of children, and not just those dealing with autism prevalence. Don't be surprised either if this in turn results in slightly higher prevalence figures.

The methodology of the NHS study is such that it doesn't leave any autistics behind, so to speak. It produces only an estimate, but it's an estimate that includes all autistics in principle (if we discount participation refusal biases.) A study that relies on a conventional screening process, on the other hand, can easily leave out autistics who did not pass the screening.

It's not easy to know a priori how many autistics a screening tool might miss. Suppose you evaluate 1000 random persons with a reliable diagnostic instrument and also a screening tool you want to test. You might identify 10 autistic people by means of this undoubtedly expensive endeavor. Suppose 5 of them also passed the screening. Can you assume 50% of autistics are missed by the screening tool? Not really. With statistical confidence, you can only say that anywhere from 20% to 80% would pass a screening.

Sure, you could test a much larger group of previously identified autistics. But how do you know this group is representative of all the autistics you intend to identify in a subset of the general population? This is clearly a limitation of pre-NHS methodology.

In the old days, they didn't even take into account the likely unreliability of screening methods. In Lotter (1966), for example, they just provided a questionnaire for teachers to fill out and only considered children reported as having "certain types of behavior." At various other levels of screening, it was always assumed the screening was perfect.

This brings me to a relatively recent study, Kadesjö et al (1999). It reported the prevalence of ASD was 1.21% in the small Swedish town of Karlstad. All children involved were born in 1985. What's interesting about this study is its intensity. The primary author personally evaluated 50% of 818 children attending normal classrooms. Unfortunately, it was a small study. They found 10 autistic children out of 826. If they had only found 9 autistic children, prevalence would be 1.1%. If they had found 11 children, prevalence would be 1.3%. I can't help but wonder, though, what might have happened if 100% of the children had been evaluated. Is it possible that at least one more autistic child would be found among the remaining 409 children who were not assessed for autism past the initial screening?

To summarize, diagnostic criteria and diagnostic methods are not the only thing that matter in a prevalence study. Case finding is also crucial, but now the NHS has introduced a methodology that could make case finding practically a non-issue.

Saturday, May 16, 2009

Why is it so difficult to find the "autism gene"?

There was media coverage recently about the discovery of the "first common" set of autism gene variants. The alleles are apparently found in 65% of autistic people. What's interesting is that they also occur in about 50% of non-autistic people. (Some sources say 60%.)

That doesn't sound like a finding that, by itself, could be practically applied to the genetic screening of autistic people. I'm not too worried about that. Additionally, autism-related studies of this sort don't replicate a lot of times.

It seems to be a very difficult problem. Why is that? I'm sure different people have different views about this.

What I was wondering is whether experts dealing with a similarly elusive problem could provide some insights of note. The problem I'm referring to is that of finding the "race gene." The following are the recommendations regarding race and genetics by the National Human Genome Center of Howard University.

1. When the human species is viewed as a whole, underlying genetic variation and expressed physical traits exhibit gradients of differentiation, not discrete units. Therefore, modern extant humans do not fracture into races (subspecies) based on the modern phylogenetic criteria of molecular systematics.
2. The biological “boundaries” between any human divisions (groups, populations, nationalities) are circumstantial and largely dependent on what traits are chosen for emphasis.
3. The demographic units of human societies (and of the U.S. census) are the products of social or political rules, not the forces of biological evolution. The names and characteristics of demographic groups can change and have changed over time.
4. Group differences in health parameters are not encoded in the human genome as part of an evolutionary pattern of divergence. Thus, differences in health or disease cannot be treated as causally related to ethnoancestral groups.
5. Genotype-environment interactions are more important in explaining group differences in health than genotype, environment, or a factor called “race”.
6. The non-existence of human races (subspecies) does not mean the non-existence of racism. Racism is the structured systematic oppression against individuals and groups defined based on physical traits that reflect an extremely limited fraction of the human genome. Racism must be addressed.
7. Individuals cannot be treated as representative for all those who physically resemble them, or have some of the same ethnohistorical ancestry. Ancestries of individuals and groups should be ascertained in order to evaluate differential expression of genetic effects.


(source)

I thought that sounded quite pertinent.

I'm not saying that it won't ever be possible to fairly accurately distinguish an autistic person from a non-autistic one by simply looking at a genome sequence. As someone with a Computer Science background, I can theoretically speculate that someone will figure out a method eventually. I just don't think it will get done by simply looking for alleles that represent statistically significant "risk" factors.

See also: Race and Genetics at Wikipedia.

Friday, May 08, 2009

Another Way to Tell the "Epidemic" in California is Bogus

There's been some renewed California "epidemic" talk recently because of a report released by California DDS (this one) despite the usual DDS disclaimer to the effect that report numbers don't represent epidemiological counts of all autistic persons in the state. Kristina discussed it and there's been some media coverage as well, with the usual Rick Rollens scare-mongering about an upcoming surge of autistic adults that the state of California allegedly doesn't have any experience dealing with. There are a number of inaccuracies and faulty assumptions in the media coverage of the report, to be sure, but I wanted to focus on one particular claim found here:

The percentage of people with both autism and mental retardation has dropped significantly, a trend that may provide clues for those trying to solve the autism puzzle.


That's not stated accurately, but in fact there has been a gradual drop in the prevalence of mental retardation within the population of recognized autistics, at least for the last 17 years. See page 20 of the report.

This is a well known fact, or at least I'd like to think it is. I've discussed it several times previously (here, for example.) It is mentioned in Gernsbacher et al. (2005) as well.

I'm sure broadening ascertainment denialists can find ways to rationalize this finding. But what if I told you that the phenomenon is not only a time-based phenomenon? It can also be observed when you compare one regional center to another. That is, regional centers with a higher administrative prevalence of autism will tend to have a lower proportion of autistics who also have a classification of mental retardation.

You know a chart is coming, but as usual I'd like to be clear as to where the data comes from, so anyone reading can double-check if they so wish. I'm using a file provided by California DDS upon request, named CDERQtrData.zip. It only goes up to January, 2006, but it contains more autism-specific information for each regional center than you normally find in the regular report. I don't have population data for each regional center (and gathering that would be a bit much for a blog post) but I will use the Autism-Epilepsy ratio as a proxy of administrative prevalence. The administrative prevalence of epilepsy in California is roughly stable (just below 0.1%) so dividing the autism caseload by the epilepsy caseload of a regional center should provide us with an adequate proxy of the administrative prevalence of autism.



The figure demonstrates an inverse association between the Autism-Epilepsy ratio and the proportion (%) of autistics who also have an MR (or unkown MR) classification. The downward trend is statistically significant with 99.6% confidence.

Now, you'll note the distribution of the dots in the chart is fairly random. I wondered why that might be, especially why the Central Valley regional center would have a low administrative prevalence of autism and a low proportion of autistics with MR.

The Central Valley RC has 9,284 clients with mental retardation as of January, 2006. That's comparable to other big RCs. Of all individuals with MR, only 247 (2.7%) also have an autism classification. This is ridiculously low. I'm sure that if someone went to the Central Valley RC and screened the individuals with an MR classification, they would find that a lot more than 2.7% of them are also autistic.

It's generally understood that there's been increasing recognition of autism in the population without mental retardation. This is what they call HFA. What's not so intuitive is that there's also been increasing recognition of autism in the population with mental retardation. Clearly, regional centers have different levels of recognition across both populations. In average, 7.7% of persons with mental retardation will have a classification of autism in California (which is still rather low.)

Let's look at what the result would be if we were to adjust the autism numbers under the assumption that every regional center should have a level of recognition of 7.7%.



That's a lot more clear, isn't it? This suggests that differences in the recognition of autism in the population with MR across regional centers are an artifact.

Thought Experiment

Imagine there's a hypothetical regional center where recognition of autism has gotten out of hand, to the point where every person who resides in the area served by the RC is classified as autistic by it. In this case the Autism-Epilepsy ratio would be about 1,000.

You'll note the first chart above has a power regression model (the formula on the upper right.) The type of model is theoretically justifiable, and I can discuss that on another occasion.

y = 32.235 x-0.4525


In the model, x is the Autism-Epilepsy ratio and y is the proportion of autistics with MR.

So what if x is 1,000? This model predicts that the proportion of autistics who have MR would then be 1.41%. This is basically what you'd expect for the general population. In other words, DDS data is entirely consistent with a cultural explanation of the differences in administrative prevalence of autism between regions.

Monday, April 27, 2009

Dr. Jay Gordon Caught Making Stuff Up?

Just when I thought I wouldn't encounter better examples of the intellectual bankrupcy of anti-vaxers, comes Dr. Jay Gordon, pediatrician to Jenny McCarthy's son, with the following anecdote:
I just saw an eight-month-old boy who got two vaccines then lost his language, motor skills, reaction to his own name and responsiveness to his 3 year old sister. This all happened three hours after a DPT/HIB combination. All previous observation and video of this little boy is normal. Lots of great video of a vibrant, talkative happy baby.

He has autism now. No proof, but the temporal proximity of the regression to his vaccines is daunting to those of us who would like more rigorous proof rather than just a collection of hundreds of pieces of anecdotal evidence. Tempting to assume causation even if only this one case/child.

Just thought you'd want to know. I usually see these kids in my office months or years after the event the parents think caused the problems. I have read hundreds of emails and spoken to thousands of parents who are certain that vaccines triggered or mightily contributed to their children's autism.

Not this time: This family came to my office just days after the vaccines, distraught that he was no longer talking, smiling, acknowledging his sister or his mom and dad and was flapping his hands a lot.

(Respectful Insolence - Comment)

Don't worry. I waited for confirmation from Orac before writing this post. Some people doubted that was actually Dr. Jay, but it is. Since he posted at 00:44 Pacific, there's some speculation he might have been drunk, but who knows.

That is monumentally absurd, isn't it?

First of all, who in the hell diagnosed an 8 month old with autism? That simply can't be done. Even an 18 month diagnosis is pushing the envelope.

Then we're supposed to believe an 8 month old "lost his language" and that this was noticed in a matter of 3 hours. Typically, 8 month old babies do not talk. This is completely normal.

In so far as responding to his own name, this is possible for an 8 month old. The "name test" is supposed to be done on the baby's first birthday, however (source).

Eight month old babies have little in the way of motor skills that they could noticeably lose, unless the baby becomes paralyzed or something like that. A baby of that age can't yet walk. He should be sitting by then. In any case, loss of motor skills is unrelated to autism, and in fact should be cause to consider explanations other than autism. If it was a really obvious loss of motor skills, I'd think the baby should be rushed to a hospital, but instead the parents decided to see Dr. Jay again in 3 days.

Enjoyment of play with other children should occur around the age of 2 years.

Hand flapping is entirely normal in infants, and it seems to me that, as a pediatrician, Dr. Jay should be aware of this. Plus, in order to hand-flap, the baby needs some motor skills.

The DTP vaccine is no longer used in the US. The DTaP vaccine is what is used. It's administered at 2, 4 and 6 months of age. Same with the Hib vaccine.

So what do we have here? Did Dr. Jay make it up completely? Perhaps this is a non-event that was blown out of proportion.

Now, I wonder, was this child vaccinated by Dr. Jay? If not, why would parents take a child with the apparent symptoms noted to a doctor who is not qualified to diagnose developmental disorders, in just 3 days? Then again, is it plausible that Dr. Jay would administer 2 vaccines in one visit?

I suppose that a pediatrician who scares parents about autism and discourages vaccination could cause them to notice things that are completely normal all of the sudden.

Saturday, April 25, 2009

Maxine Aston and CADD - A Different Level of Crankery

I'm sure readers are aware fellow blogger Alyric passed away last week. Subsequent to her passing, there has been some discussion about something called Cassandra Affective Deprivation Disorder (CADD), which Alyric had felt strongly about. (See the ASAN Petition, this post by Gonzo, and this older post by ABFH with over 60 comments.)

I have to admit this CADD thing had completely passed me by. It was only after I read the documentation related to the recent activity that I realized it pertained to yours truly in a personal sense. But I wanted to see if the claims around CADD had any merit from a more objective point of view, personal implications aside.

The Syndrome

Maxine Aston claims to have discovered a new syndrome called CADD, observed in the significant others of autistic adults. Unfortunately, the only definitions of the syndrome are found in websites and books that simply list the characteristics of the alleged syndrome. I could find no mention of it in the scientific literature.

I haven't found a "how to" on making up new syndromes. But it's possible to research how it has been done historically.

In order to define a syndrome, it's not sufficient to just come up with a list of symptoms. You have to show that it exists. Testimonials are not sufficient. Consider Kanner (1943), which defined autism for the first time. Kanner wrote the case histories of 11 autistic children in detail, based on meticulous research observations.

This was not sufficient, though. For "autism" to be considered valid, subsequent research was required. For example, if autism had been found to be the same as other constructs like mental retardation or schizophrenia, say, when you match groups by IQ, then it would've been deemed an invalid construct.

The syndrome should also have some usefulness (e.g. Does it help predict something useful? Does it help define unique needs the individual might have?)

In fact, today there's some controversy about the validity of Asperger's Syndrome, since the differences between HFA and Asperger adolescents and adults (when matched by IQ) are nearly non-existent. Asperger's could very well be an unnecessary construct. But I digress.

For CADD to be considered valid, there not only needs to be a write-up of case histories in the scientific literature, you also need to show that it is different to everything that has been reported previously. Unhappy significant others and failed relationships abound. Are the relationships with autistic adults unique in this sense, say, when matched for socio-economic status and disability in one partner? And if so (which I don't doubt is true) are they uniquely bad, or are they simply different? Can any problems be explained by lack of acceptance?

Causes

The existence of the syndrome has not been established, so it seems a little spurious to talk about causes. Nevertheless, let's look into what the alleged causes are.

As far as I can tell, "sufferers" of CADD claim that it is caused by lack of empathy and lack of emotional reciprocity in the part of the autistic significant other.

Regarding empathy, there's some recent research that shows adults with Asperger's Syndrome score lower in measures of cognitive empathy, but not in affective empathy. Persons with Asperger's actually experience higher levels of distress when observing others in distress.

These findings bring into question the means by which empathy is measured in research.

I'd also recommend reading Dr. Gernsbacher's Toward a Behavior of Reciprocity.

Symptoms

The symptoms of CADD are claimed to be essentially the same as the symptoms of Seasonal Affective Disorder (SAD), including sleeping problems, depression, etc.

Again, in order to make these sorts of claims, some evidence, perhaps in the form of a case-control study, is needed. Testimonials are not sufficient. It would also be necessary to show that the symptoms can't be explained by socio-economic status, assortative mating, or disability in the significant other.

There are more far-fetched claims attributed to Aston, like CADD resulting in cancer. I'm sure this is based on one or a few anecdotes. Since cancer is fairly common in adults (the lifetime risk of developing some form of cancer is over 40%) such anecdotes are nearly useless.

Besides, there's some evidence that psychological stress does not contribute to cancer risk (e.g. Johansen & Olsen, 1997). The matter appears to be unresolved.

Conclusion

What we have here is a syndrome that has not been shown to exist, with alleged causes that might be erroneously attributed to autism, and with symptoms that haven't been shown to be associated with the alleged causes.

Sound familiar? This is no different to crankery like "autistic enterocolitis" or "mercury-induced autism." Except the promotion of CADD has the potential to result in a lot more direct damage to the personal lives of autistic adults.

Monday, April 20, 2009

Adult Outcomes from Toronto and Utah. Then and Now.

After some recent discussion around the performance of autistics in college, I decided to read Szatmari et al. (1989). I was aware this adult outcome study looked at the academic achievements of autistics without intellectual impairment (IQ >= 70).

I found that this 20 year old paper has a lot of other information of interest. Additionally, the population it studied is similar to that of the recent outcome study out of Utah that Sullivan had written about over at LB/RB.

Even though the Utah paper is apparently not yet available, there is some information from it which we can use to compare and contrast. I thought it would be useful to go through Szatmari et al. and see how it compares to the Utah study when possible, and to other outcome studies I'm familiar with.

Group Sizes

One limitation of Szatmari et al. is that it was small. They only managed to find 16 autistics who agreed to participate. The Utah study included 41 adults.

General Outcome Assessments

Szatmari et al. doesn't really provide ratings of "good" or "very good" but a fair assumption is that half of the adults would've been given these ratings, which is basically the same thing the Utah study finds.

It also reports that 4 of the 16 (25%) might be considered "recovered." This is how the paper puts it:
If a naive individual were to meet the first four probands from Table II without knowledge of their early history, one might conclude they were essentially normal.

The Utah study reports that 6 of the 41 (15%) no longer had autism diagnoses. As Sullivan notes, we don't know if they have Asperger or PDD-NOS diagnoses.

Employment & Independence

Szatmari et al. finds that 8 (50%) were in full-time employment, 3 involving regular contact with people. Five were living independently, 10 with parents, and 1 in a group home.

In the Utah study, half had full-time or part-time employment. About half lived in group homes or with parents.

Dating & Marriage

Szatmari et al. reports that 4 individuals had dated regularly and had been in long-term relationships. One was married.

The media report of the Utah study states: "A few are married and have children. They have friends or acquaintances."

Predictors of Outcome

The usual predictors of outcome, like IQ, are noted in Szatmari et al. What I wanted to go over are some of the predictors and non-predictors, measured or qualitative, which are not well known but have been mentioned elsewhere.

On early severity as a predictor, Szatmari et al. says:
Nevertheless, the results do suggest that, for this group of HFA probands, early history explained little of the variance in outcome. Indeed, the good and poor outcome groups differed little with respect to early impairments in social responsiveness, deviant language, and bizarre behaviors.

From the Utah study:
While all participants had baseline IQs in the nonimpaired range, there was limited evidence to support the use of other early childhood variables to predict adult outcome.

About the time frame when most gains were observed, Szatmari et al. tells us that:
Parents noted that the good-outcome cases had improved considerably by late adolescence. By this age, parents felt their children were still somewhat shy and awkward but not odd or eccentric.

This is something I had previously read about in Kanner (1972):
They have not completely shed the fundamental personality structure of early infantile autism but, with increasing self-assessment in their middle to late teens, they expended considerable effort to fit themselves — dutifully, as it were — to what they came to perceive as commonly expected obligations.

And:
It was not until the early to middle teens when a remarkable change took place. Unlike most other autistic children, they became uneasily aware of their peculiarities and began to make a conscious effort to do something about them.

Szatmari et al. has something to say about the involvement of the parents:
The mothers of these probands were, however, able to advocate forcefully for their child in terms of educational and recreational resources.

A similar observation can be found in Ruble & Dalrymple (1996):
What seemed to be an important predictor of success was that whenever individuals and their families were confronted with challenges, they sought and successfully accessed various supports. For example, when families were told to "place" their young children, their parents sought and created alternatives. Some of the families were the first to push for integration in school and used their natural community and family ties to include and support their child.

College Outcome

Unfortunately, we don't have data on college attendance from the Utah study. I will go over what Szatmari et al. finds, and also some data from Kanner (1971) and Kanner (1972).

Eight (50%) of the group from Szatmari et al. had attended college or university. Seven had obtained degrees. The remaining one was beginning his second year as an undergraduate.

I find this quite interesting, statistically. As of 1990, about 42.7% of persons 18-19 in the US attended college (source). It was 38.5% for 20-21 year olds. Of course, when it comes to Szatmari et al. we're talking about Canada, not the US. Additionally, the autistic individuals came from affluent families, according to the paper. Diagnosed autistics tend to be urbanites.

Now, as of 2004, about 33% of college students in the US graduate in 4 years or less, 50% in 5 years or less, and 55% in 6 years or less. About 45% take 7 years or more to graduate, or never do (source.) I think it's remarkable that none of the autistics from Szatmari et al. who attended college had failed school at the time of the study. Only one (age 19) had not obtained a degree yet, but was still in school.

Note that the autistics from Szatmari et al. were not a bunch of geniuses by any means. The average IQ of those autistics who attended college was apparently 102 (range 86 - 110.) This is similar, probably even less than the IQ of the average college student.

They generally did not obtain graduate degrees. One had an MBA. A couple had Bachelor of Science degrees. This is probably not surprising statistically. Plus, again, the study is 20 years old.

College was a relatively adequate environment for autistics, according to Szatmari et al.
Living in residence at university seemed to make a major difference to the probands themselves. It was as if the forced confinement of living with others had a beneficial effect on their socialization. Certainly, this was a time when the probands felt most accepted by their peers. To many, these were their happiest years.

I also scanned Kanner (1971) and Kanner (1972) for mentions of autistics who had attended college. I found 7 such persons, not counting "the gifted student of mathematics killed accidentally and the young man whom we have so far lost track after 1962 when he was in college." Of the 7, 5 had obtained some sort of college or university diploma. One of them had a Master's degree in Economics. One was said to be struggling in general college, but there's no follow-up as to outcome. One was a student, doing well at university, and gifted in Math.

One issue with the Kanner papers is that they were qualitative in their entirety, so it's possible some of the autistics he saw went to college and failed, but he didn't write about that.

Comment

When you look at the outcomes of autistics who have a distribution of IQs similar to what you find in the general population, certain difficulties and impairments will be evident: autistics struggle a lot when it comes to marriage, dating, friendships, independence, etc.

When it comes to employment, we know that autistics are under-employed. It's not clear how well the autistics who are employed do at their jobs. Some qualitative data from Kanner (1972) suggests that autistics who grew up in the 1960s and who got jobs did fairly well. It's also not clear why half the autistics from Szatmari et al. were not employed.

As far as college enrollment, there doesn't appear to be much of a difference between autistics and non-autistics of the same intelligence. In fact, autistics seem to do (or used to do) rather well in college, judging by the rates of graduation reported.

Tuesday, April 07, 2009

Very Quick Note About Self-Concept and Achievement

I was looking for something else entirely and I happened to come across an old paper titled "Self-Concept of Ability and School Achievement" (Brookover & Thomas, 1964.) I thought it was pertinent to the discussion around the BRAINHE study on neurodiversity and particularly Jake Crosby's contention that self-confidence does not have an effect on "real" success. His claim was counter-intuitive all in itself. This might also be of interest to Billy Cresp, who appears to believe intelligence is the only variable that matters.

The abstract follows.

Three hypotheses concerning self-concept were tested using a sample of 1,050 seventh grade students and a selected subsample of 110 over- and under-achieving students. A significant positive relationship was found between self-concept of ability and grade point average; this relationship persisted even when measured intelligence was controlled. Specific self-concepts of ability related to specific areas of academic achievement were found; in some areas these were better predictors of achievement in the subject than general self-concept of ability. Self-concept was significantly and positively related to the perceived evaluation of significant others. A direction for further research is indicated.


(Emphasis mine)

Monday, April 06, 2009

One Handley Turd I Left Out

In my previous post I looked at a few statements JB Handley made during his recent appearance on Larry King Live. Whether the statements were dishonest or simply wrong, I can't tell, but they were notable in their wrongness. They have even been referred to as fractally wrong.

I left an important one out, which I was pretty sure was wrong, but I needed to research it a bit more.
So I would tell you either go back to the 1989 schedule before this whole mess happened or go to Finland's schedule, Sweden's schedule, Norway's schedule and use theirs. Because their autism rates are one tenth of ours.

He must mean their rates of identified autism are one tenth of what they are in the US. I don't like it when people don't make that clarification.

But let's see what a quick search of the literature has to say.

Sweden

One study in the town of Karlstad, Sweden (Kadesjö et al. 1999) had found the prevalence among 7 year olds to be 1.21%. I'll let Lorna Wing summarize why this study is of interest:
Kadesjö et al (1999) report a study in Karlstad, a Swedish town. Although this was small scale it was very intensive (over 50% of the 7 year old children seen and assessed personally by the first author). The study found a prevalence for all autistic spectrum disorders for all levels of IQ, of 1.21%!!! Children were followed up four years later and had the diagnoses confirmed.

That's not all, though. You have, for example, Arvidsson et al. (1997), a study that set out to identify "all individuals with severe degrees of autistic behaviour." They found a prevalence of 31 in 10,000 among 3 to 6 year olds. This is more like half of the consensus prevalence in the US.

Then there is Gillberg et al. (2006) which finds a prevalence of 20.9 in 10,000 for autistic disorder, and 32.9 in 10,000 for "other ASDs." That's 53.8 in 10,000 total.

There are several other studies from Sweden we could look at, but I think the wrongness of Handley's claim has been clearly established just with the ones mentioned.

Finland

Mattila et al. (2007) found a prevalence of 25 in 10,000 for Asperger's Syndrome alone. This is actually higher than what the prevalence of Asperger's in children is normally found to be.

An older study, Kielinen et al. (2000), finds a prevalence of 20.7 in 10,000 among 5 to 7 year olds. This is lower than the US consensus prevalence, but it's only 1/3rd of it, not 1/10th. Additionally, note that 50% of the children had IQs below 70. This is different to what you see in California DDS, for example.

Norway

The most recent epidemiology from Norway is a bit old, and here we do see that the prevalence is similar to what it traditionally was for Kanner autism. For example, Sponheim & Skjeldal (1998) find a prevalence of 4 to 5 in 10,000 for 3 to 14 year olds, using ICD-10 criteria.

However, there's a recent screening of 7 to 9 year old children using the ASSQ. That's Posserud et al. (2006). It finds that 2.1% of children were high scorers in the ASSQ when both teacher and parent questionnaires were considered. (It was 2.7% if they considered teacher forms only, as some parents declined to participate.) That seems high.

Unfortunately, Posserud et al. don't tell us how many were confirmed to be diagnosable with ASD after the screening. There's an update of that study, Posserud et al. (2009). I wish I had a copy. All I know is that the ASSQ is found to have a sensitivity of 0.91 and specificity of 0.86, which appears good.

In any case, JB Handley's assumption is kind of simplistic even if we only consider the country of Norway, as it ignores all the issues involved in identifying autism.

Saturday, April 04, 2009

JB Handley - Poorly Informed or Outright Liar?

Last night I was changing the channel and I stumbled upon Larry King Live (transcript here.) It must have been only a couple of minutes before they switched to Anderson Cooper. During that time, I got to watch JB Handley make a monumentally false statement. I'll go over several statements he made during the show, but first I want to address the one that caught my attention.
Did you see the January study from UC Davis using California's numbers that said unequivocally there's been a clear rise, it's not do [sic] to diagnostic substitution.

Handley is referring to Hertz-Picciotto & Delwiche (2009). This is what the conclusions of the paper actually said:
Autism incidence in California shows no sign yet of plateauing. Younger ages at diagnosis, differential migration, changes in diagnostic criteria, and inclusion of milder cases do not fully explain the observed increases. Other artifacts have yet to be quantified, and as a result, the extent to which the continued rise represents a true increase in the occurrence of autism remains unclear.

That's not an unequivocal determination of a clear rise, by any stretch of the imagination. Besides, that paper was surprisingly poor. None of the figures used by the paper approach anything that might be called certain or accurate. One of the artifacts the paper fails to take into account is probably the most pertinent artifact of all: awareness. A summary of all the very serious problems the paper had can be found at the end of this post.

Next statement:
We're looking for something that's caused this epidemic. It went from one in 10,000 in the 1970s to less than one in 100 today in many states.


The first epidemiological study of autism was Lotter (1966). It finds a prevalence of 4.5 in 10,000. That was in the UK. Wing et al. (1976) finds the same prevalence in the US. Mike Stanton has a good summary of historical prevalence studies. I don't think this is the first time I've corrected Handley and others about this.

I happen to have read Lotter (1966). What they called 'autism' back then is very different to, say, what the DSM-IV calls 'autism' today. It's apples and oranges. Here's a excerpt from Lotter (1966) to give you an idea:
The two categories of the Creak criteria concerning a "'pathological preoccupation with particular objects" and "an insistence on the preservation of sameness" were therefore combined.

These are similar to criteria C2 and C4 of the DSM-IV, but in the DSM-IV they are basically optional (only 1 item from C is required.)

The paper explains they located 666 out of 75,930 (88 in 10,000) children who had "certain kinds of behaviour" that couldn't be simply characterized as "backwardness." They initially excluded 87% from this group, based on the opinions of two judges familiar with the syndrome of autism.

They ended up with 32 autistic children, 22 (68.8%) of whom had IQs under 55, another 5 (15.6%) with IQs between 55 and 79, and the remaining 5 (15.6%) with an IQ of 80 or above. Again, this is quite different to what we call 'autism' today.

Moving on:

I want to talk about this issue of autism prevalence. It's going to be shocking for parents to learn that the CDC and the AAP don't actually acknowledge that there's been a real rise in autism cases. Larry, the Department of Education in 1992, 16,000 kids were getting autism services. Today 225,000. That means in 1992, they were missing 93 percent of kids with autism. Where are all the adults with autism? They don't exist.


Adults with autism don't exist? That's not only insulting and potentially damaging to the quality of life of autistic adults; it's completely wrong. It becomes embarrassingly wrong every time someone goes and surveys adults to see if autism can be found among them.

Again, I doubt this is the first time this has been pointed out to JB Handley.

Heck, Handley's Age of Autism has a token autistic adult who contributes to that blog from time to time.

His Special Education figures are essentially correct, except the year is 1993, not 1992. What he fails to mention is that 489,000 students were receiving services under the mental retardation category in 1993, and only 425,000 as of 2007.

Let's consider Specific Learning Disability and MR together, and let's also consider population growth. The prevalence of both categories combined was 645 in 10,000 in 1993, and 584 in 10,000 as of 2007 for 6 to 17 year olds. That's a drop of 61 in 10,000 – more than enough to cover the increase in the administrative prevalence of autism.

Is it possible that JB Handley has never heard of diagnostic substitution in IDEA? Doubtful.

Those are all the statements I will address in this post. Readers are welcome to point out other errors, if any.

My impression is that JB Handley is either completely misinformed about some basic facts having to do with autism epidemiology, or he decided to go on Larry King to simply lie with a straight face.

To conclude, here's some advice for Larry King: In the future, if you want to discuss the "autism epidemic," you would do well to invite recognized experts on the matter, such as Roy Richard Grinker or Eric Fombonne.

Friday, April 03, 2009

Autism Awareness and its Relationship to the "Epidemic"

Yesterday was World Autism Awareness Day. (That's right, its acronym is WAAD, and it's the day after April Fool's day.) Given the occasion, I thought I would discuss "awareness." More specifically, I wanted to discuss how we can tell that awareness has had an impact in what is usually referred to as the "autism epidemic."

That awareness could account for much of the increase in autism diagnoses since the early 1990s is taken for granted. You will find awareness mentioned in many autism papers. In the recent MIND Institute paper (Hertz-Picciotto et al. 2008) awareness was acknowledged but not taken into account in the calculations. While H-P et al. apparently did not believe awareness to be an important factor, many other researchers seem to think it is. I personally believe it's supremely important. Changes in criteria can't in themselves cause the number of diagnoses to rise. Autistic persons need to be found and diagnosed (with autism) before they are counted. If diagnostic substitution is increasingly occurring, there's probably a reason why it's occurring: awareness.

Nevertheless, as far as I know, no one has ever demonstrated that awareness explains the rise, statistically. Thus, we fall into the same trap that proponents of most environmental hypotheses fall into. We assume that because awareness has increased in the information age (as it obviously must have) and rates of autism have also increased, one causes the other. Could it simply be a coincidence?

How do you measure awareness? Here's one way. I will use Google News Archive Search to search for the phrase "autism california" every year from 1992 to 2006. I propose that the number of results is an adequate proxy of autism awareness in California, though like all proxies, it's just an approximation.

I'd like to have data on diagnoses of autism to be able to make a comparison. I don't have that, however. Here's the next best thing. I will use data on number of California DDS clients with a classification of autism as reported on March of every year from 1993 to 2007. More specifically, I selected the number of autistic children born only 3 years prior to the report.

Let me explain the rationale. If we were to choose 5 year olds, that wouldn't work very well, as they could've been diagnosed when they were 2, 3, 4 or 5. It would be difficult to correlate caseload in the report year with awareness in several prior years. If we instead choose children born only 3 years before the report year, they almost necessarily have to have been diagnosed the year prior to the report year. This is especially true if we use the March report. If we were to use the December report, this again might not work very well.

Without further ado, the following is the graph I came up with.



The blue line represents awareness. The green line represents autism caseload of 3 year olds, approximately. There are 2 Y axis scales, left and right respectively. I think the 1 year lag between one and the other is pretty clear. If you prefer to visualize the data in a scatter chart, here it is:



It's true that correlations that are purely coincidental (e.g. pirates vs. global warming) can result in convincing scatter charts like the one above, and I haven't done further statistical analysis to rule out coincidence, but I think there are a couple of clear features of the series that make me think we're looking at causation. First, I already noted there's a 1-year lag in the expected direction. Second, awareness seems to start to shoot up in 1999. Autism caseload, in this cohort of very young children, starts to increase noticeably in 2000. Then there's also a clear spike in awareness in 2005, which corresponds to a spike in caseload in 2006.

Considering there's also plausibility, I think we can safely say awareness did have an impact in the rise of autism diagnoses. I only looked at very early diagnoses, but this is because I don't think I have other data that could be adequately used instead. I would imagine awareness has an impact on diagnoses at any age.

Wednesday, March 11, 2009

This is not a Parody of Dan Olmsted. This is Actually Him.

From Age of Autism:
Olmsted on Autism: Man Kills Ten, Self. Why?
Aluminum poisoning
By Dan Olmsted

It's way too early to conclude anything about the reason behind yesterday's rampage in Alabama, in which a man killed his mother, 9 others and himself. But it is not too early to point out a couple of facts.

First, the place he chose to end his life was the parking lot of a former employer, Reliable Products in Geneva, Ala.

Second, according to Reliable's Web site, "Reliable Products is the leader in louver manufacturing for the thru-the wall a/c and heating industry." All these products -- grilles, louvers, vents -- appear to be made of aluminum. Reliable is, in essence, an aluminum products manufacturing facility.

Aluminum, as we know, is toxic ...


What's the standard response in these situations? Oh yeah...



For background, see this post.

Wednesday, March 04, 2009

AoA's Token Aspie Reacts to BRAINHE Study With Error-Filled Article

Anti-vaxers have a lot to be upset about lately. First, it turns out that Wakefield probably falsified his data. Second, they took a beating scientifically and legally at the Omnibus Autism Proceedings. Third, their attempt to counter-attack by recycling a weak vaccine injury case from 2007 and acting as if it were new and "hidden" did not bear fruit.

To top it off, they've recently come to realize that neurodiversity is actually studied by scientists and sociologists. To be clear, neurodiversity is not the opposite of anti-vaccination. One has little or nothing to do with the other. Anti-vaccination has to do with causation, science, autism quackery and public health. Neurodiversity is a social concept, essentially independent of causation, which is not exclusive to autism by any means. Anti-vaxers, nonetheless, see neurodiversity as a threat for various reasons that are beyond the scope of the post.

In my last post I wrote about the BRAINHE Project report on neurodiversity. There's one paragraph in the report that I think is worth quoting again.

13 of the participants viewed their neurodiversity as an entirely negative matter. These participants frequently used negative or medical terminology when talking about their labels which indicated that they felt in some way broken or damaged. Of the 13 students who had this view, 8 indicated low academic self-esteem and expressed confusion and uncertainty about their future plans. Participants who viewed their neurodiversity as a difference which included strengths were more likely to have higher academic self-esteem, to have experienced unpleasant epithets from teachers and to have a clear ambitious view of their future.


Jon Mitchell reacted to this report, and I already discussed that. It's not surprising that AoA'ers would also react. To do that, they brought out their token Aspie, one Jake Crosby, who writes for AoA from time to time. I hadn't heard of Jake Crosby previously, but I guess we can add him to the short list of autistics who actively oppose neurodiversity, and who always happen to be high functioning.

Jake Crosby's article, titled "The Age of Neurodiversity," is filled with errors. I'm saying it's filled with errors because I'm giving Mr. Crosby the benefit of the doubt. I could just as easily have said it's filled with lies and misrepresentations. Any other major blog (or "internet newspaper") would be embarrassed to publish an article with these many inaccuracies. Let's go over some of them.

[Paul Offit] strangely cites two neurodiversity moms, Kathleen Seidel and Camille Clark for medical evidence, neither of whom have any medical background.


I've read False Prophets and my instinct was that Mr. Crosby was mistaken. I read it again just now, and at no point are Kathleen or Camille cited as experts who provide medical evidence. They are in the book simply to show that not all parents of autistic children are anti-vaxers.

He would simultaneously oppose any alternative therapy or pathological theory for autism, however effective or true, even if it is on the basis of what a few ND moms say.


I haven't seen any evidence that Dr. Offit would oppose any "pathological" theory of autism. Reading False Prophets gave me the opposite impression. As most doctors, he most likely sees autism from a purely medical perspective.

As to opposing "alternative" therapies that are "effective and true," that's an oxymoron. If a therapy is shown to be "effective and true," it's no longer an "alternative" therapy. It's simply a therapy. There's no evidence that Paul Offit would oppose therapies that are "effective and true." In fact, he seems to favor ABA because he's been led to believe it's effective, even though he is, in my view, mistaken in that regard (as high quality evidence on the effectiveness of ABA is lacking.)

In his final chapter, "A Place for Autism," Offit continuously touts the views of the five autism parents he dedicates his book to, the majority of whom believe in neurodiversity while the remaining have pharmaceutical industry ties.


Other than Kathleen and Camille, Dr. Offit's book features Peter Hotez, Professor of Microbiology and Tropical Medicine at George Washington University School of Medicine; and Dr. Roy Richard Grinker, Professor of Anthropology at George Washington University. I don't know about Dr. Hotez, and doctors are obviously bound to have connections to the pharmaceutical industry (just as, say, the Geiers do) but I seriously doubt Dr. Grinker has such ties.

This is strange, as apparent confidence or career ambition does not dictate real success or happiness.


This is a perplexing statement. It does not make sense, first of all. If you have zero confidence and zero ambition, it's improbable you will achieve much, regardless of how smart you are.

More importantly, there's a significant body of science on the effects of self-confidence on success, failure and performance. Mr. Crosby might want to read up on that before making statements that are nonsensical.

After a closer look of the study, “Student experiences of neurodiversity in higher education: insights from the BRAINHE project,” I quickly noticed that not all the people in the study were autistic. For one, it was published not in a journal about autism, but dyslexia. In fact "Dyslexia" is the name of the journal. It was not even focused on autism.


This discovery is kind of funny. It shows that Mr. Crosby has no idea what neurodiversity is. As the word suggests, neurodiversity is about, you know, neurological diversity. It's not a concept that is married to autism. The fact that neurodiversity as a term was coined by autistics and is most often discussed in the context of autism is of interest, but ultimately immaterial. It's good to see that researchers are applying the term broadly, as they should.

This is how the researchers define neurodiversity:

Neurodiversity is an umbrella term for many types of learning difference.


The study is about neurodiversity, not about autism. I'm not sure what's so hard to get about this.

Furthermore, this study does not contribute to how prevalent the idea of "Neurodiversity" is within the autistic community because this study examines six autistic people.


So? However prevalent the idea of neurodiversity is among autistics now, what the results of the study tell us is that it's in everyone's best interest for it to be more prevalent among anyone with a learning difference. From the study, it appears that the split on views is about 50/50 among those with learning differences.

Presenting it as if it reported that autistic students and graduates adhere to neurodiversity is a misrepresentation within the article that cited it.


The article that cited it was actually quite critical of neurodiversity. At no point did it make it sound like most autistic students adhere to neurodiversity. That's simply a fabrication. The following is what the article said.

According to recent research, people with autism who accept the neurodiversity platform have more self-esteem, and have more academic and career ambition that those who see autism as a medical condition with its array of disadvantages. In one study, students with autism who held the latter view more often applied for special assistance and monetary allowance through disabled students programs. Not surprisingly, most neurodiversity advocates with autism are high functioning, with little to no significant intellectual impairment.


I don't know if Mr. Crosby was pressured to produce his critique, and had a hard time coming up with proper arguments to refute the research in question. Either way, his critique is a complete disaster, and frankly, he should be embarrassed.