California’s sevenfold increase in autism cannot be explained by changes in doctors’ diagnoses and most likely is due to environmental exposures, University of California scientists reported Thursday.
The scientists who authored the new study advocate a nationwide shift in autism research to focus on potential factors in the environment that babies and fetuses are exposed to, including pesticides, viruses and chemicals in household products.
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Unfortunately, it’s a poor study. It resolutely refuses to consider the notion of diagnostic substitution, (the fact that the overall number fo children needing services is relatively consistent, although the labels change). Here’s a good paper from Psychological Science in the Public Interest that’s speaks directly to this point.
http://www.psychologicalscience.org/pdf/cd/autism_epidemic.pdf
It’s a really, really crappy study you’re hawking here, I’m afraid:
See:
http://www.theness.com/neurologicablog/?p=454
And more:
http://autismnaturalvariation.blogspot.com/2009/01/mind-institutes-second-attempt-more-of.html
Posting is different from endorsing. Though Orac can do no wrong, since I read his blog.
At least the actual source article included some of the graphs. If the quotes from the researchers are accurate and indicative, they do not seem to be supported by the published research. The fact that the greatest rate of change occurred in the 2-3 yo. group is even more troubling to me. How the hell do you apply the DSM-IV criteria to a 2 year old. It seems nearly incomprehensible that a behavioral syndrome is being diagnosed at such an age. If someone suggested diagnosing 3 year old children with depression I should hope they would he soundly laughed out of whatever positions they held.
Does Orac disagree with Dr. Bernardine Healy’s contention that the practice of thimerosal containing flu vaccines is a possible environmental inducement of autism that should be investigated?
Does Orac disagree with the UK (Bromely, Mawer, Clayton-Smith, Baker) study showing that children born of mothers given the epilepsy drug valproate were seven times more likely to develop autism than children born to mothers who took no epilepsy drug while pregnant?
Hahaha,oh Greg,
did you realize what sort of can of worms you were opening LOL
Without getting into the nitty-gritty of the trench wars on autism here,I ask everyone to just think about the diagnosis of ADHD and depression in children,and the incidence of these conditions since we started diagnosing them.Every kid that forgets to memorize a poem for class and instead goes riding his bike in the backyard is diagnosed with ADHD these days.
Same goes for autism.
And the nutters on both side of the trench are not helping to rationalize the dabate.
My understanding was that Orac disagrees with the kooks’ contention that the repeated investigations that have been undertaken thus far and failed to support a causal link should be thrown out and the investigations repeated until statistical noise produces a result that is to the kooks’ liking.
Wow! I am truly astonished at the dismal quality of most of these comments. Come on people, we can do better than that. I know nothing about this issue, and a two minute inspection allows me to discover that most of you are speaking out of an orifice other than your mouth. Let’s review.
stewart: Are we allowed to read only the first page of that paper? Anyway, it is simply not the case that the study refuses to consider changes in diagnostic rate. It IS, in large part, a study of changes in diagnostic rate. If you want to claim that changes in diagnostic rate against an otherwise stable background rate is the explanation for the documented trend, then pleas do so in a way other than waving a magic wand. The study makes explicit statements about this that you are free to mention and disagree with. That would be better than just saying it is not there. Right now you are sounding like a kook when you say that. Please revise.
Orac: Hawking? Bite me. You know, sometimes I think it is really too bad for all those kids who should be getting vaccines that you are on their side. They deserve better. Thanks for the links to the blog posts, though, that was nice. Let me know if you have something substantive to say about this study, I’d love to hear it.
Robert S.: That is not the source article you are linking to. You note: “they do not seem to be supported by the published research.” I just want to verify that you can’t say this without having seen the published research. You may be right, but you would have to look at the published research before actually knowing if you are right. Regarding the age and diagnosis issue, you’ve got nothing. The typical mildly or poorly informed member of the public often believes that early diagnosis of whatever (fill in blank) is impossible or too difficult because they can’t imagine how it is done. Until I see something more from you I’m going to assume that this is the case with your statements. Feel free to correct me if I’m wrong about that.
Harold: I am not a this moment familiar with the studies you (sort of) cite, but I can ask this: Do they look at interaction effects? Is there not a likely similar cause for the condition for which the mothers are treated and the autism in the children? You seem to be more engaged in a fight with Orac (which I can understand … he invokes those feelings with his lovely style) than a discussion over the cause of autism. The cause of atuism is more important than your ego or Oracs. Can we try to get on the same page here?
clinteas: I’m not so sure. Kids these days ARE doin’ it wrong, as kids in EVERY generation have! Don’t you think?
Azkyroth: That seems to be correct, but what about the possibility that the accepted methods are inadequate for all of the possible demand of research? For instance, isolating causes is at the base of almost all research designs, at some level, but this makes it difficult to study interactions.
Did you read Orac’s second link?
I wish I had access to the full text of the study, because the Natural Variation blog post suggests that the study didn’t directly evaluate diagnostic substitution at all. From the blog post:
How do the study authors justify their assumption that diagnostic substitution rates in California over a decade or more are numerically identical to those in two Finnish provinces over a 2 year period?
Give me a break with the self-righteous whining. You posted a link to a story on a study without comment, and the implication tends to be that you find it interesting and may even believe its results, especially given the excerpt you chose to post. You don’t think it’s worthwhile? Then write something–anything–about it, other than the “link and excerpt.”
Come to think of it, you’re one to talk about not having something substantive to say about this study when you yourself didn’t bother to–oh, you know–actually say something about it. Pot, kettle, black, dude. At least I provided links to good skeptical discussions of the study to support my characterization that it’s a bad study. Indeed, I consider those discussions so good that, given that both bloggers beat me to discussing this study, I decided that I didn’t have much to add.
Yes, I do disagree with Healy, who has turned into a bit of a crank over the last couple of years. Multiple large, well-designed studies have failed to find a detectable association between thimerosal-containing vaccines and autism. Scientifically, it’s a nonissue. In fact, even antivaccine activists realize it’s a losing issue, and that’s why they’ve changed to the “toxins” in vaccines gambit or the “too many too soon” mantra.
Orac: Ignoring for the moment your irrelevant ranting about how and what I should blog, I have a serious question for you: Why would the shift from vaccines to “toxins” in vaccines have any wind at all? Isn’t the real killer study regarding the vaccines based on the idea that there has not been a downward shift in autism rates since the most yecky of the toxins was removed from vaccines? Is it the case that the autism = vaccines link is really mainly an anti-vaccine phenomenon that is exploiting autism rate increase (real or perceived)?
BTW, I had not read the original paper because when I looked for it in the journal, it was not there. I had not realized it was published in the last full issue (I was expecting it in the forthcoming section.) I’ve got it and I’m reading it.
Greg, this will sound crass, but evidently you don’t. Let’s see:
Stewart mentioned diagnostic substitution. The study does not look at diagnostic substitution at all. It looks at changes in diagnostic criteria, age of diagnosis and inclusion of “milder” cases. Is diagnostic substitution part of changes in diagnostic criteria? Not necessarily. I argue that in my critique.
Of course, a more general way to explain what’s missing from the paper is that it does not consider awareness, as the researchers admit.
Furthermore, the paper explains a 4.26-fold rise. It claims this means they cannot account for 6.85-fold rise. How so? Where’s the range of statistical confidence?
Interestingly, the paper claims the impact of diagnostic criteria alone is precisely 2.2-fold. This comes from a single Finnish study, and the researchers use this in favor of the results of a meta-study claiming that the impact of criteria is 3.6-fold. If H-P et al. had used the 3.6 figure, they would’ve explained all of the rise (102% to be precise).
I’m about to talk mostly out of my ass, here goes:
You know there is a third possible explanation for the rise besides statistical or environmental. That’s that the cause of autism is genetic, but that human mating habits have changed in recent decades to promote some genetic disorders. There are recent studies that demonstrate changes in partner selection by women taking birth control over women not taking the pill. These changes certainly have implications regarding the immune system. It possible there are other effects, as well.
Before feminists jump on me, understand I’m totally with you, and I fully understand the implications of that statement. This is worth studying, and if turns out to be true, the proper response is to reevaluate how birth control is used, and to investigate non-hormonal forms of birth control for both men and women.
I would suggest that all interested people read the actual, published paper at:
http://www.vetmed.ucdavis.edu/cceh/Epipaper1208.pdf
The tone is completely different from that of the press releases.
Oooh, Orac and Greg going at it!
*sits back and munches popcorn*
Jennifer: Yes, the tone is totally different. This paper is being slammed by people who, sadly, seem to know what they are talking about but will take this paper down because there is the possibility that it can be interpreted as opposed to their opinion. Which, in my opinion, is more interesting than the paper itself. The paper is OK, a step forward in some areas, good and flawed at the same time, but not as interesting as the debate itself, in this case!
Joseph: The study at hand considers diagnostic substitution at a number of points. It is not the main focus.
I completely disagree. I think people have been too kind to the paper, perhaps because it’s not a paper by cranks. Frankly, I would’ve expected a paper like this from the likes of the Geiers.
The only novel result from the paper is the 1.2-fold rise due to age of diagnosis. (I would caution this should not be interpreted as age of diagnosis not having changed much – that’s the change in the proportion of diagnoses by age 5).
The other results are recycled from elsewhere.
They use a single Finnish epidemiological study to come up with the figure on the impact of diagnostic criteria. It’s a complete stretch to suggest that the results of that study might be applicable to California DDS ascertainment between 1990 and 2006. Are we also to believe it’s precisely 2.2-fold and it can’t be a little higher?
It’s true that the paper uses appropriately skeptical language at times. I mean, it has to. But you should see what the primary author said to the media.
Honestly, if they wanted to raise funds for environmental research, there are probably better ways to achieve that. Calling autism an epidemic has many non-trivial moral and economic implications. False epidemics solicit false causes and waste research money.
So, Joseph, your criticism is then mainly with the media side of this? There is a very different slant when comparing the paper and the UCD press report (go read the whole thing, don’t base anything on my little quote). And when we go one further step out into media land the fundamental nature of the paper is almost entirely lost, and it looks like a paper specifically asserting that there are specific environmental causes.
But that happens to all papers all the time. No need to single this instance out as unique in this regard.
Greg, its quite obvious that Joseph *has* read the paper. Its equally obvious that when you posted this blog entry, you had not. I’m going to quote you something from the paper and then something from CDDS. See if you can spot the problem:
H-P:
CDDS (private email)
Can you see the problem with this paper yet?
Obviously, it’s not mainly that. What I’m saying is that the paper should not be given a pass just because it uses some skeptical language, when the authors (and others) clearly want to communicate that this is a definitive study proving the “autism epidemic.” For reference, this is how Dr. H-P is quoted by WebMD.
I took that from Autism Street, BTW, where you’ll find yet another post on the matter, primarily looking at diagnostic substitution in California, which incidentally is hard to deny once you look at an aggregate of all special education categories.
Greg: You are correct that I had not been able to find an accessible copy of the paper that the article commented on. However, if you read to the end of the article you linked to you would find that it was a reprint. After seeing that I found the original article (commenting on the paper in Epidemiology 2009;20:84-90) and found the reprint was without the graphs. I was unclear in my language regarding the press article vs the published paper which probably lead to my comment being misunderstood.
Now that I have read the paper (thanks to Jennifer), I do have a problem with one of the conclusions made in the discussion section. They never seem to allow for early incidence not corresponding to the expected prevalence that might occur if the developmental delay was temporary. A very brief and shallow look at pubmed suggests that at least some children would no longer qualify under the diagnostic criteria if evaluated later (e.g. PMID: 17206522). Significant changes in the training of pre-k teachers in California has taken place since the last full birth cohort (1996). If nothing else it will be interesting to see if the conclusions drawn will correspond with the data as it develops over the next few years.