Friday, May 29, 2009

Griswold's Conjecture

For the time being, I am going to name the following statement Griswold's Conjecture:

Employment of early intervention for children diagnosed with autism leads on average to poorer outcomes than would have been the case without such intervention.

For the purpose of this conjecture, “early intervention” is defined as any technique administered to autistic children with the intent of ameliorating or removing autistic behaviors and attributes. Examples would include applied behavioral analysis, pharmacology and chelation.

I am uncertain if anyone else has attempted to state a similar hypothesis (and if they have, I will gladly rename the conjecture), but I believe it is important to place this statement as formally as possible within the autism debate arena; for at the present moment, the autism research community is unabashedly assuming its negation. In nearly every research article and in nearly every accompanying press release, autism scientists can be heard repeating the mantra that early intervention greatly improves outcomes for autistic children. The correct reply to such statements should be, “Really? So you have disproven Griswold's Conjecture? Can you show me your results?”

With increased awareness and diagnosis of autism, it has become more and more apparent that in the past most autistic individuals went entirely unrecognized. Therefore, many of these individuals would have been raised in circumstances similar to non-autistic individuals, and would not have been exposed to intervention techniques designed to lessen or remove their autistic characteristics. Although specific outcomes would have varied greatly, statistics make it clear most of these individuals did not end up in institutions or in other similarly poor circumstances. In all likelihood, many of these individuals—perhaps a sizeable majority—somehow made their way into general adult society, more or less indistinguishable from the other members of the population.

Today, circumstances have changed greatly. More and more autistic children are being exposed to early intervention techniques targeted specifically to the amelioration or removal of autistic behaviors and attributes, and there is a growing body of anecdotal evidence suggesting these techniques lead to very poor outcomes (see for instance here, here and here). Without further investigation, it remains unclear whether early intervention does not in fact produce exactly the opposite result from what the autism research community intends, does not produce a very large increase in negative outcomes for autistic individuals.

Therefore, I am placing this challenge before the autism research community: disprove Griswold's Conjecture, or else quit assuming its negation.

Saturday, May 23, 2009


Another of Derrida’s non-identical twins.
So many approachable works—
Like a stash of Chrysler building replicas
Fashioned from styrofoam blocks.
(And it must be admitted,
There is a certain amount of talent
Required for a portfolio like that.
And it must be admitted,
The graduate school audiences
Prefer their buildings that way.)

Of course the trouble with approachable works
Is they dare an approach,
And up close,
We see no business is ever conducted in a building like that—
No elevators rising and falling,
No boardroom dramas between dusk and dawn,
No graphite pencils ground to their messy point.
Up close,
It resembles not a building at all—
For that, one keeps a safer distance.

Far removed from campus,
The child without siblings,
The child without peers,
Dares to slice the styrofoam to ribbons,
Crushes the blocks for pellets,
Burns the plastic down to goo,
And beyond that flotsam books uncertain passage
Over fathom-rich seas.
Searle (your brethren too)—
It is of no use to craft life preservers
From the material of a philosophy professor’s chair.

Thursday, May 14, 2009

Ray of Light

From the darkness known as IMFAR 2009, there appears to have emanated at least one small ray of light. In a poster presentation entitled The Level and Nature of Autistic Intelligence II: What about Asperger Syndrome? (Mottron, Soulières, Gernsbacher, Dawson, 2009), the Mottron team adds further detail to its previous paper The Level and Nature of Autistic Intelligence (Dawson, et al., 2007), this time demonstrating that individuals with Asperger Syndrome (defined as individuals diagnosed with some form of autism, but without presentation of various forms of communication difficulties) evince the same pattern of Raven's versus Wechsler intelligence scores as was demonstrated by the autistic population studied in the 2007 paper.

I do not want to make too much of an abstract from a poster presentation, but the findings here are important in at least one respect. Much of the response to the 2007 paper focused on the idea that the Raven's test is essentially non-verbal, with the suggestion being that the better performance of autistic individuals on the Raven's test could be accounted for by the fact that Raven's bypasses autistic language difficulties, whereas Wechsler does not. That suggestion, however, is misleading, and the 2009 poster presentation reveals the flaw, for it demonstrates that in general all autistic individuals—with strong verbal abilities or not—show a similar pattern of test results. This means that something more than just verbal strengths and weaknesses is being captured in the autistic pattern of Raven's/Wechsler intelligence scores.

In my opinion, the differential performance of autistic individuals has far more to do with the question domain of the respective tests than it has to do with whether the tests are “verbal” or not: the question domains of some tests match well to autistic intellectual strengths, the question domains of others do not. Tests like Raven's and the block design subtest of Wechsler contain questions built strongly around pattern recognition and structural manipulation—a type of question that matches well to the non-biological, pattern-oriented focus that is characteristic of autistic perception. The questions of the other Wechsler subtests (comprising quite the hodge-podge) in varying degree are less pattern oriented, and they also tend to contain more culturally derived elements, elements that autistic individuals are perhaps less likely to perceive with ease.

These intelligence studies, spearheaded mostly by Michelle Dawson, are quite simple in scope and design, but they have revealed an unexpected result (at least, unexpected by the autism research community): autistic intelligence is much different in kind than non-autistic intelligence, and autistic intelligence cannot be explained away by assuming it is nearly the same as non-autistic intelligence, with just an assortment of defects tacked on.

This is a good occasion to highlight the unique role Michelle Dawson now occupies within the autism research community. Ms. Dawson is unlike any other researcher in autism's now vastly overcrowded field—for Ms. Dawson does not possess a slew of post-graduate degrees, Ms. Dawson has not patiently worked her way up through the hierarchical ranks, Ms. Dawson has not been shedding pieces of her scientific soul in order to remain part of the gathering throng. Ms. Dawson's presence in the autism research community is due almost entirely to her autism and to her intelligence, and due to the fact that Laurent Mottron has had enough discernment and courage to recognize Ms. Dawson's talent and vision and to incorporate her efforts into his research team's work. The results have been electrifying, for the Mottron team is now the only autism research team to have moved firmly away from the autism-as-disorder orthodoxy and to have provided valuable insights into the nature of autistic individuals as they truly are. The entire Mottron team deserves credit for these many contributions, but it also clear the inclusion of Ms. Dawson has had a catalyzing effect.

When will the rest of the autism community learn the importance of this lesson?

Inclusion of autistic individuals leads to intuitive, hard-to-see-otherwise insights about the nature of autism. Exclusion of autistic individuals leads only to a continuing blindness.

Monday, May 11, 2009

In Response to Harold Doherty

I am responding to Harold Doherty's post here, because Mr. Doherty has been known to edit and censor comments on his own blog.

It is important to note that I am not describing Deborah Fein's study as “fictitious,” I am describing Mr. Doherty's version of it as fictitious. The description in Mr. Doherty's original post does not appear to match any presentation made by Dr. Fein at IMFAR 2009. Mr. Doherty has picked up phrases from media reports, such as “years of intensive behavioral therapy,” and made them an actual part of Dr. Fein's study/presentation, when in fact it appears there is no basis for doing so. He then uses this pseudo study as “evidence” in support of the effectiveness of applied behavioral analysis (ABA). Dr. Fein appears to have provided no such evidence.

Mr. Doherty is correct in that Kristina Chew appears to have made the same assumptions about Dr. Fein's study as Mr. Doherty has. Ms. Chew, on the other hand, has not been so adamant about employing such assumptions as “evidence.”

I think Michelle Dawson has the best advice for all of us. Drawing conclusions from media reports and abstracts is a dangerous business. I will admit to some frustration about the general inaccessibility of much autism research, but it still behooves those of us who wish to participate in the autism debate arena to make sure we have as much accurate information at our disposal as is reasonably possible.

That said, I stand by my original assessment: Mr. Doherty's description of a particular ABA/recovery study does not appear to match any such study. Mr. Doherty is free to provide a link to that study if he really wishes to engage in “evidence.”

[Update 05/16/2009: Be sure to read these observations and informative discussion from someone who actually attended Deborah Fein's presentation at IMFAR.]

Sunday, May 10, 2009

Harold Doherty's Fictitious ABA Study

You have to give Harold Doherty credit for trying. Apparently flummoxed by the lack of real autism science in support of applied behavioral analysis (ABA), Mr. Doherty has responded by concocting an ABA study pretty much out of thin air.

Mr. Doherty's technique this time was to lift some random words from a Washington Post article in order to create the following description of a study presented at this year's International Meeting for Autism Research (IMFAR): “a study was presented at an autism conference by University of Connecticut psychology professor Deborah Fein showing recovery of between 10 and 20% of subjects originally diagnosed as autistic who were later determined to have lost the autism diagnosis after years of intensive applied behavioral analysis.”


Both a perusal of the Washington Post article and an examination of search results from the IMFAR conference reveal that no such study exists. Deborah Fein did make a presentation at IMFAR regarding a study describing the various characteristics of children defined as “recovered,” but that study was not a long-term study of children under intensive ABA treatment, and that study did not draw any conclusions about the effectiveness of various forms of treatment. Nearly everything in Mr. Doherty's description turns out to be the product of his overactive and not very insightful imagination.

But here is the real irony: if Mr. Doherty's fictitious study were in fact an actual study, it would have devastating consequences for Mr. Doherty's own ABA advocacy. The problem, of course, is that a 10-20% recovery rate is a shockingly low number. The history of autism diagnosis, in which the vast majority of autistic individuals once went entirely unrecognized (and thus by Deborah Fein's definition, would have to be deemed as fully recovered) would suggest the corresponding recovery rate under no treatment at all runs significantly higher than a mere 10-20%. Thus, it would appear the use of ABA on the children in Mr. Doherty's fictitious study has had a tragically negative effect.

Here would be my suggestion to Mr. Doherty: the next time he decides to gild the ABA lily, perhaps he should do a little more gilding in favor of his own side.

[Update 05/16/2009: Be sure to read these observations and informative discussion from someone who actually attended Deborah Fein's presentation at IMFAR.]

Saturday, May 9, 2009

Katie Wright and the Autism Time Machine

On the surface it would appear Katie Wright and I have much in common. We each have a son (of nearly identical age) who is autistic, and we each have been less than impressed with the goings-on at IMFAR 2009. Perhaps I should consider ringing up Ms. Wright so that we might share our similarities over a cup of coffee.

Except...we share no similarities.

In the first place, one of us has a son who is regarded as being as near to perfect as he can possibly be, a true blessing to be enjoyed for every single one of his traits, including—and indeed, most especially—his autistic traits. The other has a son who seems to be regarded as little more than a set of inflamed bowels.

And as for IMFAR, although I can certainly agree with Ms. Wright's assessment that IMFAR's scientists have become stuck in a kind of treacherous time warp—a spinning of the same gerbil's wheel again and again and again—my suggestion would be not to set the time machine back to an era of voodoo and the traveling medicine show, but instead to try something astonishingly new, to envision autistic individuals as people not disordered or diseased, to respect them for exactly who they are, to encourage them to thrive as they were autistically meant to be. Since this approach has not been tried in the past or in the present, I think it would be safe to call it a treatment for the future.

But Ms. Wright would rather we overthrow all the stale neurobiology, genetic studies, mice models, pharmacology, and all the rest, by substituting instead chelation alchemy, lupron elixers, anti-vaccination incantations and biomedical binging. “Eye of newt and toe of frog, wool of bat and tongue of dog”—that would appear to be the formula most befitting Ms. Wright's logic and modernity.

As I suggested to Mark Blaxill, that other Age of Autism denizen, if Ms. Wright really wishes to gain some insight into why the autism community—and I mean all the autism community—seems to be so stuck in time and unable to forge ahead, perhaps she should consider how much she actually has in common with all those IMFAR scientists she mistakenly supposes are on the opposing team. What she and they share are the conviction that autism is a dreadful disease, a terrible disorder, something in need of being cured, destroyed, eradicated, and if Ms. Wright really wishes to know why the entire autism community has become so irretrievably mired in a thickening mud, there can be found her backwards looking answer.

So instead of ringing up Ms. Wright for that cup of coffee chat, I would rather leave her with just a simple message: the substitution of one set of atrocities with a different set of atrocities is not the same thing as making progress.

Wednesday, May 6, 2009

IMFAR 2009

This week sees the annual gathering of autism researchers known as IMFAR (International Meeting for Autism Research). These conventional affairs always carry the danger of being rather dreary occasions, but judging from the 2009 program guide, it would seem a spirited attempt has been made to jazz up this year's event by casting it into a bacchanalic celebration of everything autistically dysfunctional—noxious neurobiology, genetic degeneracy, molecular malfeasance, morbid comorbidity—a veritable gorge-fest of autism as disorder and disease.

I am uncertain when science will eventually turn in favor of autistic individuals, and be no longer lined up against them—certainly not soon enough for my own taste—but when science does begin to make that turn, I hope the names of Lord, Bear, Scherer, etc. are not then quickly forgotten. Mass ignorance is no excuse for the atrocities being spewed forth by such researchers, for indeed, where do we think mass ignorance originates. From the very beginning, there were unmistakable signs that autism-as-defect was inaccurate, harmful and prejudicial, and researchers such as Lord, Bear, Scherer, etc.—no matter what excuses they may happen to give—they have simply chosen to ignore those signs.

When science eventually does make that turn, let us have the courage to look back in a kind of sickening wonder, look back on that lugubrious jubilee known as IMFAR 2009.

Monday, May 4, 2009

Thanks. Now Here Is the Back of Our Hand.

It is amazing how articulate autistic children can be, and just as amazing how dense and cruel autism research scientists can be in response.

A little more than a month ago, press releases were circulated regarding the results of a report published online by the journal Nature, Two-year-olds with Autism Orient to Non-social Contingencies Rather than Biological Motion (Klin, Lin, Gorrindo, Ramsay, and Jones, 2009). Here is the report’s introduction:

Typically developing human infants preferentially attend to biological motion within the first days of life. This ability is highly conserved across species and is believed to be critical for filial attachment and for detection of predators. The neural underpinnings of biological motion perception are overlapping with brain regions involved in perception of basic social signals such as facial expression and gaze direction, and preferential attention to biological motion is seen as a precursor to the capacity for attributing intentions to others. However, in a serendipitous observation, we recently found that an infant with autism failed to recognize point-light displays of biological motion, but was instead highly sensitive to the presence of a non-social, physical contingency that occurred within the stimuli by chance. This observation raised the possibility that perception of biological motion may be altered in children with autism from a very early age, with cascading consequences for both social development and the lifelong impairments in social interaction that are a hallmark of autism spectrum disorders. Here we show that two-year-olds with autism fail to orient towards point-light displays of biological motion, and their viewing behaviour when watching these point-light displays can be explained instead as a response to non-social, physical contingencies—physical contingencies that are disregarded by control children. This observation has far-reaching implications for understanding the altered neurodevelopmental trajectory of brain specialization in autism. This study points in a number of interesting directions.

The report goes on to describe this study in more detail, outlining how autistic children and control groups were shown side-by-side videos of point-light animations formed from scenarios played out by human actors, with one display being shown right side up and forwards running in time (so that the light points had some resemblance to human motion), the other display being shown upside down and backwards running in time (so that the light points had a fairly random appearance and were not synchronized to the accompanying sound track). Using eye gaze as a measure, the non-autistic control groups were shown to have more preference for the right-side-up display, whereas the autistic children were shown to have no particular preference for one display or the other. This was apparently the initial purpose of the study, to show that non-autistic children have a normal, and therefore “healthy,” response to biological motion, whereas autistic children do not: one more wood chip on the autism-as-disorder lumber pile.

However, in one of the trials, where the human actor was playing pat-a-cake (with the clapping sound prominent on the sound track), the researchers noticed that a fifteen-month-old autistic girl—who in the other trials was showing preference for neither of the displays—was in this case evincing a clear and intense preference for the upright image. Since it was only in the upright image that the clapping sound corresponded to the motions of the point-light display, the researchers wondered if it was the synchronized clapping that the autistic girl was responding to, and after re-examining all their data—and after developing further trials to confirm their “serendipitous” discovery—the researchers concluded that a preference for non-biological pattern was consistent and significant across the entire autistic study group. The overall findings of the study were therefore greatly enhanced, such that they could be summarized in the following manner:

  • Non-autistic toddlers respond preferably to human biological motion, and do not respond preferably to non-biological pattern.
  • Autistic toddlers respond preferably to non-biological pattern, and do not respond preferably to human biological motion.
  • Neither group responds preferably to random sensory noise.

To be honest, these findings are not nearly as new as the report’s press releases would have us believe—they are consistent with many other findings regarding the primary distinctions between autistic and non-autistic perception—but the study’s enhanced conclusions are at least more valuable than they would have been based on what the researchers initially had in mind, for the enhanced conclusions provide a more accurate picture of what autistic perception naturally is, as opposed to just another worn-out description of what autistic perception is not (not to mention, the enhanced results add to our knowledge about non-autistic perception as well). It would seem, therefore, that the study’s researchers owe a debt of gratitude to that articulate autistic girl who pointed them in the right direction, for it was after all she who helped them see what had actually been in front of their eyes all along.

And how did the autism research community decide to repay this debt of gratitude? Why, it repaid this girl in the same fashion autism researchers have always responded to articulate autistic children—by giving her the back of their hand.

Here is a sampling of quotations given in response to the Klin, et al. study:

From Ami Klin, the study’s lead author: “Our hope is to detect vulnerabilities for autism as early as possible, so as to intervene with the hope to capitalize on the babies’ brain malleability.”

From Thomas Insel, Director of the National Institute of Mental Health: “For the first time, this study has pinpointed what grabs the attention of toddlers with ASDs [autism spectrum disorders]. In addition to potential uses in screening for early diagnosis, this line of research holds promise for development of new therapies based on redirecting visual attention in children with these disorders.”

From Geraldine Dawson, Chief Science Officer for Autism Speaks: “These findings could potentially be useful in detecting infants at risk for autism very early in life. It is important to use therapeutic strategies for children with autism that help draw their attention to people, including their facial expressions, and gestures.”

So let me see if I have this straight. This young autistic girl and her study group cohorts helped open the researchers eyes to the fact that autistic individuals do not have randomly damaged perception, but instead respond positively, consistently and usefully to a particular form of stimulus in their environment, and the researcher’s only response to this discovery is to suggest forcible removal of the preferred form of perception from autistic children and to offer instead mass substitution of the one type of stimulus autistic children have markedly demonstrated they do not respond to. Absolutely amazing. If I were to suggest that non-autistic children could be greatly improved by forcibly redirecting them away from biological and social stimuli and towards a non-stop bombardment of pattern-based perceptions while their brains were still malleable enough to be re-formed, I would be derided for both my folly and my cruelty. But somehow, when the corresponding approach is suggested for autistic children, that is considered the height of scientific insight!

If we could just capture stupidity on point-light displays, then I am sure autism research scientists would show a 100% preference for exactly those images.

I hope one day, after that articulate autistic girl has had time to grow up and come to understand the blind-aping world in which she lives, she manages to track down those so-called scientists Klin, Insel, and Dawson, and in the literal manner autistic individuals are apt to prefer, gives them the back of her hand. The intellectual and moral bankruptcy of the autism research community has reached an all-time peak.

Friday, May 1, 2009

Naturally Hilarious

I often feel compelled to poke fun at the autism research community, but sometimes I have to wonder why I bother, since that community does such an excellent job of making itself look ludicrous.

Case in point: this week's “big” autism research news (not to be confused—although it is admittedly hard to do—with all the previous weeks' big autism research news) is occasioned by the publication of two articles in the journal Nature (Common genetic variants on 5p14.1 associate with autism spectrum disorders (Wang, et al., 2009) and Autism genome-wide copy number variation reveals ubiquitin and neuronal genes (Glessner, et al., 2009)), along with all the ballyhooed press releases that inevitably accompany such weekly big news. In these two articles, the authors put forth their latest findings on genetic risk factors that “likely” account for autism: a barely significant genetic variant found at 5p14.1 (different of course from all the previously announced and much ballyhooed genetic variants), and a mixed bag of copy number variations (different of course from all the previously announced and much ballyhooed copy number variations). We can rest assured, however, that these particular genetic breakthroughs are of great importance—even if by my count they bump the number of such genetic breakthroughs well into the hundreds—because we have the assurance of all the authors and several leading experts that these breakthroughs account for as much as 15% of all autism cases, which means (adding this percentage to the percentage of autism cases accounted for by all the previously announced genetic risk factor breakthroughs) the autism genetic research community has now managed to account for as much as 7000% of all autism cases. Well, yes indeed, that would be a cause for celebration—and of course more press releases.

To get a sense of just how much of a caricature all this autism genetic breakthrough news has become, note that Mark Blaxill—he of SafeMinds and Age of Autism fame—has quite nicely and quite accurately poked a hole in this latest celebration balloon by simply resorting to some simple common sense—and this from a man who does not possess any common sense! If that alone does not give the Nature studies' authors a profound sense of shame, I am not sure what will.

But it gets more laughable still, for now we come to the matter of Geraldine Dawson, Chief Science Officer of Autism Speaks. Dr. Dawson, as it turns out, is a co-author on both the Nature articles (which, as I will discuss below, is not quite the statistical fluke it would seem). What is amazing to me is how Dr. Dawson's name keeps popping up week after week under the heading of so many widely varying autism research ideas. As was discussed here, Dr. Dawson has recently celebrated nearly all the vastly different autism research achievements published in the year 2008, highlighting the great hope and the great promise to be found in all sorts of studies attributing autism to such things as genetic location 16p11.2, pesticides and insecticides, as well as the birth months of April, June and October. But then early 2009, Dr. Dawson has reappeared as the co-author of a paper lending support to hyperactive amygdalas as the definitive explanation behind the mysteries of autism. And now this week...Dr. Dawson has come out as lending her support to genetic location 5p11.4 and a new batch of copy number variations. Talk about hedging one's bets! I get the feeling that although Dr. Dawson is not certain which big autism breakthrough is going to win its research team the Nobel Prize, Dr. Dawson has become absolutely convinced she needs to be associated with that team.

To be honest, I am going to have to quit mocking Dr. Dawson over her profligate support of each and every autism discovery that comes down the pike, because quite frankly it has become tedious. Let me end with an obvious conclusion: whatever autism's big research news might happen to be next week (and the week after that, and the week after that, and the week...), we can rest assured Dr. Dawson will somehow be found nearby, hovering at the edges of the celebration, all too happy to have lent a supporting word and, of course, her co-authorship.

And yet, as hard as this might be to believe, I have saved the most ridiculous feature of the two Nature articles for last. The most ridiculous feature is that the first article has 56 co-authors and the second article has 59 co-authors. You read that correctly—56 and 59 (although come to think of it, you might want to check my arithmetic—it is difficult for me to count that high without making a mistake). When I first noted this exponentially increasing trend of piled-on co-authorship in autism research papers, and challenged the autism research community to create an article in which the list of authors was longer than the report itself, how was I to know the autism research community would take me so seriously! But indeed, that community is now coming nearer and nearer to its goal, because this time, I actually had to get out a ruler and measure the print to be sure. Alas, even disregarding the lengthy list of references (fifty-some authors citing their own works does take up a bit of space) and disregarding the equally lengthy list of acknowledgements (although tell me, exactly how much work is required to merit an acknowledgement in one of these papers, given that such work does not qualify for even 1/59th of the authorship credit)—even disregarding all these tacked-on supplements, the list of authors still does not quite exceed the length of the report itself. Sorry, folks, thanks for playing, better luck next time! (For its next effort, might I suggest the autism research community try reducing the size of the report's charts and graphs, or better yet, strive to achieve the century mark in co-authorship—a feat which, at the rates things are going, can certainly be attained by later this year.)

Yes indeed, Nature was certainly the correct place to publish these two articles, for they are naturally hilarious.


Mark Blaxill has written an extraordinary piece for the Age of Autism web site entitled Latest Autism Gene Studies Find...Not Very Much. If one ignores the unconvincing and completely unnecessary smears of Paul Offit and the Children's Hospital of Philadelphia, what remains is a mostly cogent, well-supported argument for why the two recent publications in the journal Nature (Common genetic variants on 5p14.1 associate with autism spectrum disorders (Wang, et al., 2009) and Autism genome-wide copy number variation reveals ubiquitin and neuronal genes (Glessner, et al., 2009)) should be taken with a very large grain of salt. Mr. Blaxill's examples are on point, are well-documented, and through them he manages to debunk nearly all the hoopla surrounding the Nature articles and to place these articles in a more critical and useful light. He accomplishes all this by applying just some simple common sense.


Where in the hell did Mr. Blaxill acquire any common sense? This is the same man who most assuredly informs us that autism is caused by vaccines and other environmental toxins, and will answer our skepticism by calling us liars, morons and shills. If we hold our ground, and insist upon some tangible corroboration, he will trot out unpublished study after unpublished study, each one more fantastical than the previous, each one not a worthy enough companion for any genetics-based stretch of credulity that might be found on the pages of Nature. The same man who rightly points out that when one genetic study implicates 16p11.2 as the likely risk locus for autism, and the next study implicates 5p14.1 as the likely risk locus for autism, and the next study implicates fill-in-the-blank as the likely risk locus for autism, then perhaps all this talk about genetic risk loci for autism is not quite as promising as it first appears—this is the very same man who one day claims it is thimerosal that definitively causes autism, the next day claims it is the measles virus that definitively causes autism, the next day claims it must be aluminum that definitively causes autism...the common illogical thread apparently lost on him. Extraordinary.

If Mr. Blaxill really wishes to engage in some common sense thinking, might I suggest he begin by examining the connection linking the autism genetic studies he so thoroughly excoriates, and the autism-vaccine hypothesis he most assuredly espouses. Each approach begins with the assumption that autism is a dreadful disease, a terrible disorder, something in need of being cured, destroyed, eradicated. If Mr. Blaxill really wants to discover where all the autism woo begins—and I mean all the woo—there can be found a common starting point.