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01 Jan 2010
  • Author: Sullivan
  • Comments: 71
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Autism Clusters Found: areas with high incidence of autistic children

Researchers at the U.C. Davis MIND Institute has discovered regions in the state of California that have notably higher autism incidence. But the story is more complicated, and more sad, than one might think at first. Instead of indications of an “autism epidemic”, these clusters point to the fact that minority and poor children are much less likely to receive autism diagnoses.

I don’t have the paper yet (I’m still trying to find the abstract), but articles in the Woodland Daily Democrat and the San Diego Union-Tribune are reporting the story.

The clusters do not appear to point to environmental causes. Instead…well, read for yourself:

Researchers said that in this investigation the clusters probably are not correlated with specific environmental pollutants or other “exposures.” Rather, they correlate to areas where residents are more educated.

Children with autism diagnoses in these clusters are more likely to be White and have parents with high education levels. Again, a quote:

“In the U.S., the children of older, white and highly educated parents are more likely to receive a diagnosis of autism or autism spectrum disorder. For this reason, the clusters we found are probably not a result of a common environmental exposure. Instead, the differences in education, age and ethnicity of parents comparing births in the cluster versus those outside the cluster were striking enough to explain the clusters of autism cases,” said senior author Irva Hertz-Picciotto.

Kids in the “clusters” are about twice a likely to be diagnosed autistic and kids in nearby areas.

Twice as high.

To the many of us armchair epidemiologists who who have looked closely at the California Department of Developmental Services (CDDS) data, this comes as no surprise.

For me, the most memorable discussion of the autism clusters came from Autism Diva, in her post from July 1997, Malibu and Compton: Compare and Contrast.

Here is a graph from that post:

The South Central Regional Center, in a predominantly non-White, poor area of the Los Angeles basin, had an administrative prevalence of 33 per 10,000. Compare that to Westside Regional Center with a prevelance of 84. Westside is a much more affluent are with a higher proportion of White families.

From the San Diego Union-Tribune:

“There is mounting evidence that at least some of this clustering results from the greater access and utilization of services by those with more years of schooling,” the UC Davis researchers wrote.

Yes, there is a certain “I told you so” moment here. This blog, Autism Diva, Autism Natural Variation, Autism Street and others have been pointing out the apparent autism clusters in the raw CDDS data for years. Long before I started blogging. But the real story isn’t the effect such clusters have on the idea of the “autism epidemic”. Rather, this is a clear indication that we are underserving the disabled in our minority and poor communities. This is just plain wrong.

It is long past time for real autism advocacy organizations to work on increasing awareness and access to services in underserved areas. The autism “clusters” are probably not real. From where I sit, what is real are the “anti—clusters” of undiagnosed autistics, minorities, the poor, and, yes, adults.

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Comments

71 Responses to “Autism Clusters Found: areas with high incidence of autistic children”


  1. Tom
    January 1st, 2010
    07:37:52

    From the American Journal of Epidemiology (2003) Article entitled “Infant Sleep Position and the Risk of Sudden Infant Death Syndrome in California, 1997-2000” by Li, Pettitti, Willinger, et al.:

    Sleep position of Control infants

    White Infants
    62.2% put to sleep on their backs

    Hispanic Infants
    51.6% put to sleep on their backs

    African American Infants
    42.4% put to sleep on their backs

    If we willingly accept that sleep position can have such a profoundly positive impact on SIDS rates can we at least consider that it may also have some profound negative effects also?

    Infants who sleep supine compared to infants who sleep in the prone position are impacted in the following ways: – Social skills delays at 6 months (Dewey, Fleming, et al, 1998) – Motor skills delays at 6 months (Dewey, Fleming, et al, 1998) – Increased rates of gastroesophageal reflux (GER) (Corvaglia, 2007) – Below norm AIMS scores (Majnemer, Barr, 2005) – Milestone delays (Davis, Moon, et al., 199 – Increased duration of sleep apnea episodes during REM sleep at both 2.5 months and 5 months (Skadberg, Markestad, 1997) – 6% decrease in sleep duration (Kahn, Grosswasser, et al.,1993)

    – 1 in 300 infants had plagiocephaly in 1974 (Graham, Gomez, et al., 2005) – 1 in 60 infants had plagiocephaly in 1996 (Graham, Gomez, et al., 2005)
    “Infants with deformational plagiocephaly were found to have significantly different psychomotor development indexes and mental developmental indexes when compared with the standardized population.”
    Kordestani, et al. in their study “Neurodevelopmental Delays in Children with Deformational Plagiocephaly”

    “There are indications of a rapidly growing population of infants who show developmental abnormalities as a result of prolonged exposure to the supine position.”
    Dr. Ralph Pelligra regarding the impact of the Back to Sleep Campaign
    http://cgi.thescientificworld......reamweaver

    “Since the implementation of the “Back to Sleep” campaign, therapists are seeing increasing numbers of kindergarten-aged children who are unable to hold a pencil.”
    Susan Syron, Pediatric Physical Therapist

    “In its fundamental purpose it has been largely successful. The incidence of SIDS has been reduced dramatically. However, as many orthotists can attest, this important gain has not been without its lesser comorbidities. The one we tend to think of has been the rapid increase in the incidence of positional plagiocephaly and positional brachycephaly. However, there have been whispers and rumors of other effects.”
    Phil Stevens, MEd, CPO regarding side effects of the Back to Sleep Campaign.
    http://www.oandp.com/edge/issu.....-12_02.asp

  2. [...] This post was mentioned on Twitter by Jack Scanlan, autism_hub. autism_hub said: New post: Autism Clusters Found: areas with high incidence of autistic children http://bit.ly/4RYkdQ [...]

  3. The social inequality is the key factor.

    Convergent data , see also this :

    Texas Study Confirms Lower Autism Rate in Hispanics
    “Autism could be under diagnosed among Hispanics, Palmer and his team note, given that these children are less likely to have health insurance and more likely to have trouble accessing medical care.”

    http://abcnews.go.com/Health/wireStory?id=9441843

    The debate ‘inequality link’ vs ‘environmental link’ seems to be nearly closed.

    What is interesting in information genealogy is how statistics are used.

    And information genealogy is the best way to avoid time vaste in false links.

  4. LB/RB “underserving the disabled in our minority and poor communities. This is just plain wrong.”

    “@ageofautism: Why do rich white kids have more autism? Does CAVIAR cause autism???”

    “@ageofautism: Autism Centers spring up where there is autism and in areas where folks can afford the treatment. ARGH!”

  5. My favorite historical cluster, for geographic reasons, is Brick NJ in 1998. The ingredients? A less than 5 year old IDEA legislation; add one heaping helping of an active special needs parent group called ‘Parents of Special Services and Education’, mix in complete cooperation of the schools, health care to records, and bake with the comparatively unlimited resources of the federal government to gather and analyze data. The result: a ‘cake’ that mirrored autism rates 10 years later.

    That’s why I have some trouble with the ADDM data on an individual state basis. Too many ‘cooks’ making their cakes in different ways. Their data pieces may be the same, but the politics, demographics, psycho-social, and educational policies may be vastly different.

  6. The question is how many of these minority and “under-served” kids are diagnosed with other conditions, other than autism. For example, we discovered in our area, white kids were diagnosed with autism, and minority children were diagnosed- with the same presentations- as mentally retarded. In special education, we had disproportionality with autism (percentage of white children high), mental retardation (black children high) and emotional disturbance (black and hispanic children high). The good news was that minority children were being given support services- the bad news was they were being mislabeled, and those labels can impact a child’s future throughout adulthood, changing what opportunities are made available and what services can be accessed.

  7. Hi Sullivan –
    I saw this, thanks for posting it.

    Considering that there are many more poor people than rich people, what happens to our prevalance numbers once all of these people get evaluated and diagnosed? Even by only counting the rich people, we seem to have reached the number of one percent that is fundamental to the argument of a static incidence of autism.

    – pD

  8. Even by only counting the rich people, we seem to have reached the number of one percent that is fundamental to the argument of a static incidence of autism.

    That’s a good question. It will go over 1%, I believe, first of all.

    Now, it’s true that administrative prevalence of ASD can be much lower in counties with low population density. I’ve analyzed this using California IDEA data, and the correlation is roughly logarithmic and quite good.

    What would happen if all those counties started counting all autistic children? Probably not as much as might seem intuitive at first glance, depending on the state. Note that in California about 90% of the population appears to be an urban population.

    Additionally, IDEA prevalence and CalDDS prevalence are nowhere near 1%. (This San Diego study, like all MIND studies, are probably based on samples of children from CalDDS.) IDEA reports available list autism when it’s a “primary disability” only. The phone survey uses a completely different counting method. The ADDM data is based on specific sites.

    So basically, special education and service databases seem to undercount a lot more than other methods, and they have a lot more room for growth. I do think IDEA prevalence could in theory reach Minnesota 7 year-old levels across the US (1.4% or so), which would be a huge jump, but the increase won’t be as pronounced when you use other counting methods.

  9. This isn’t surprising at all. Socio-economic class dictates that middle-class white Americans are going to get services and diagnoses while poor minorities are going to lack that.

    Duh. It’s basically stating the obvious. Only people that can afford it, get diagnosed. So what are we going to do about it? Should we start planning out systems to get free diagnostic care for the poverty class? As well as systems in place for poor working classes to get services for their autistic child? Because here is another idea. If poor folks can’t afford diagnosis, what makes you think that they can afford ABA, OT or Speech therapy?

    We what should we tell the government?

  10. The UK doesn’t seem to be as good at collating this sort of data (taking Joseph’s points into account) but it should be noted that if I recall, the UK study that found a prevalence of 1% was concentrated in (I believe) a very affluent area of London. It would be interesting to see a study in an area with a much less well educated and well resourced area of London as well.

  11. To further elaborate on pD’s question, I looked at some county-level IDEA data from a few years back (that I believe I got from Sullivan.)

    Admin prevalence for the state as a whole was about 50 in 10,000. The most dense counties (LA area) have a prevalence of about 60 in 10,000, which is not that different than the state as a whole. This is even though sparsely populated counties have a prevalence as low as 1.5 in 10,000 (e.g. Inyo county.)

    CalDDS is probably going to work in a similar manner. The most densely populated counties will dominate state prevalence, despite ridiculously low prevalences in sparsely populated ones.

    To put it another way, if the researchers did this San Diego study in the Los Angeles area, their findings will probably not be as strong.

    If all counties caught up with the LA area, prevalence would only increase 1.2-fold.

  12. This is even though sparsely populated counties have a prevalence as low as 1.5 in 10,000 (e.g. Inyo county.)

    I need to correct that. It’s about 8 in 10,000 for Inyo, which is still quite low. I was looking at the wrong column. Alpine county had an IDEA prevalence of zero, but its population is only 1,261.

  13. Liz,

    I gave myself a gift this Christmas—a few days not reading AoA!


  14. Bill
    January 1st, 2010
    20:55:51

    Does it ever occur to anyone that since much autism/Asperger’s is genetically based, that it is quite possible that some races may naturally have a higher incidence? We wouldn’t dare say the white community is underserved because they don’t have enough sickle cell anemia clinics, would we?

  15. Does it ever occur to anyone that since much autism/Asperger’s is genetically based, that it is quite possible that some races may naturally have a higher incidence? We wouldn’t dare say the white community is underserved because they don’t have enough sickle cell anemia clinics, would we?

    It is possible. For example, if I recall correctly, Dr. Fombonne found a lack of autism in the Innuit. The possible “Amish Anomaly” could be genetic, especially considering the dramatic rise in vaccination uptake in the past 20 years.

    However, there are some studies which have discussed prevalence amongst racial groups. Those studies showed a lack of variation by the races they studied, as I recall.

    But, if there are races that have higher incidence or lower incidence, why do they all seem to be increasing in administrative data? If

    It is well worth studying if there is a variation by race. First, we need accurate numbers (which educational and services data like CDDS are not). Until then, the responsible thing to do is assume that the prevalence values are the same as the highest found. Seek out those who may be getting the wrong or even no support.

  16. I think it should be higher priority to study if there is true variation by region. For example, do counties like Inyo really have fewer autistic children? This is the sort of thing the IACC should be doing as a prelude to environmental factor research. In other words, test the assumptions first.

  17. First of all I do not agree that this year is 2010 (I don’t even agree it is a year necesseraly) But putting such pernicketiness aside I shall tackle Sullivan.

    Fombonne would not recognise autism if he saw it face to face, the reason, it is a cultural construction.

    It is no accident that the demographics of Kanners originals was very waspish leading to rather odd conclusions at the time.

    Heck it is all cultural and it is no surprise that Kuru does not exist in the UK but new variant CJD does.

    It used to be said that the best cure for Schizophrenia was a trip accross the atlantic (can’t recall which direction but I am not perfect)

    If one believed the statistics one might well assume that in the UK there was something particular about Afro Caribean genetics that led to a higher rate (being cagey about incidence and prevelance here that ain’t relevant cos tis disputed) of Sz in that population.

    Well it does not take an Einstein to say something is rotten in the state of Denmark there (sorry I forgot that Greenland is still part of Queen Margarethe’s domain.)

    I suggest that Eric Fombonne is a latter day Lord Franklin to an anthropologist Amundsen, who could tell him that he wouldn’t know Inuit Autism if it shat on his shoes.

    BTW the no autism amongst the Amish myth has been busted I believe.

  18. Dr. Fombonne never published a paper about the Inuit, did he? I can’t find one, anyway.

    If you recall, the preliminary finding was nothing more than a database search. In other words, the Inuit don’t get psychiatric diagnoses for autism that get coded in a database – that’s all.

    I wonder what happened to that research. My impression was that there would be a follow-up effort with proper case-finding. Did it not get done? Were the results not as interesting as the researchers hoped? Is it still ongoing?

  19. “Kids in the “clusters” are about twice a likely to be diagnosed autistic as kids in nearby areas”
    This looks like it should be “than kids”.
    I suggest an experiment to test a suspicion I have voiced before: Check whether poor areas with lower reported autism rates have correspondingly higher “retardation” rates.

  20. Check whether poor areas with lower reported autism rates have correspondingly higher “retardation” rates.

    I can tell you this is not the case in the San Diego RC. It is the case in other RCs. San Diego has a relatively low prevalence compared to LA, but the prevalence of autism in the population with MR is not low. It was 9.26% as of Q4 2005, which was comparable to LA RCs.

    This means that the missing autistics are “high functioning.”

    In CalDDS RCs, I’ve observed that recognition of autism in the populations with MR and without MR do not necessarily correlate. I have an analysis related to this. I see in it that the Central Valley RC is an example of an RC with very low recognition of autism in the population with MR (2.7% as of Q4 2005.)

  21. Let’s not forget that clustering can occur because some districts provide better services (or, simply services) than others, so people move to those areas. In other words, they’re not sources of autism causes but of autism effects!

  22. Hello friends –

    Does it ever occur to anyone that since much autism/Asperger’s is genetically based, that it is quite possible that some races may naturally have a higher incidence?

    This occurred to me in regards to the very strange Somali cluster in Minnesota. A lot of the African cultures are still highly tribally based, as was the basis of the genocide in Rhwanda. Anyways, it occurred to me that one possible reason we might see more Somalis in one area with autism, but not in others was that individuals from a certain tribe, with consequent genetic likenesses, relocated to Minnesota and encountered an environmental input.

    – pD

  23. Let’s not forget that clustering can occur because some districts provide better services (or, simply services) than others, so people move to those areas. In other words, they’re not sources of autism causes but of autism effects!

    It appears that the study looked at place of birth for the clusters, not place of current residence. That should remove the possible bias you mentioned.

  24. At its most fundemental the problem is that people are using the wrong measurements.

    The CDC is the wrong instrument for any objective estimates of prevelance in that it is not an academically designed instrument with checks and balances, it is a political statistic, and a heavily socially nuanced one as well, as has been clear for some time.

    It is like trying to use a tachometer to measure the speed of a car when the speedo has failed, unless you understand the underlying mechanism and ratio of the gears rpm tells you nothing.

    One thing is always the case, a small sample is always a skewed sample because it is not large enough to contain every eventuality that occurs in nature.

    Given that autism as concieved statistically is a medical diagnosis in the context of a very haphazard system of social practice.

    Current systems can’t even get a realistic prevalence of swine flu right because there isn’t independant confirmation that every case reported is not seasonal flu.

    So much more difficult it is with autism, a socially defined condition without rigid boundaries, whose diagnosis (and the very word means opinion in itself) is driven by clinical opinion, based upon individual contexts and conditions that vary according to the families status and knowlege as much as the clinicians status and experience.

    Autism itself is partly the fault, it is a syndrome, a collection of symptoms not a distinct entity with a discrete biomarker.

    Put it another way, if I were to emigrate to California, and never seek a service, how would my UK diagnosis impact on the statistics if at all?


  25. Visitor
    January 2nd, 2010
    13:28:38

    Another issue, which I’ve never seen discussed, is the effect of advocacy at local level. If the nationwide stats say 1 in 110 children have an autistic spectrum disorder, but in Lincoln county only 1 in 60 have been diagnosed, then one can infer that pediatricians may come under pressure of some sort (possibly even from their own desire to do the best) to lower the threshhold, or in some other way find children, so as not to leave unaddressed needs. This would potentially be a particular issue as the importance of early identification is increasingly recognized.

    This, in turn, will push up the national stats, next time around.

    Am I wrong to wonder about this?

  26. I find it difficult to believe there could be any children with Kanner’s Autism unknown to the authorities under some guise or another.

    All I can see is a mish-mash of different definitions, methodologies and screening instruments, with little standardisation across different studies and groups. It appears futile to try and extract anything useful that can be stated with conviction.

  27. Passionless Drone, did it ever occur to you that the genetic basis of autism is but a hypothesis wanting any decent confirmation.

    There is no absolute genetic code for autism, there are no consistent findings, only a range of studies indicating totally different morphologys.

    This indicates if anything that there is no genotype of autism and that what is labled together as a “syndrome” has a variety of etiologies.

    Does it never occur that looking for genetic causes for Cancer, there is no ‘cancer’, only cancers.

    One is essentially looking at the genetics of Unicorns.

    The differences we see in diagnostic rate are social constructs.

    Indeed I believe that over time when the various genetic studies have either been replicated or not, it will become clear how much of a construct autism is, and we will be looking at it more in the way that one looks at the concept of race itself.

    Autism is a complex phenomenon as complex as personality and a long way from being simplified or understood in medical terms.

    You are all on the road to defeat. The tragedy is that people will be eliminated on the basis of the current unsound genetics.


  28. David N. Andrews M. Ed., C. P. S. E.
    January 4th, 2010
    07:27:05

    “If the nationwide stats say 1 in 110 children have an autistic spectrum disorder, but in Lincoln county only 1 in 60 have been diagnosed, then one can infer that pediatricians may come under pressure of some sort (possibly even from their own desire to do the best) to lower the threshhold, or in some other way find children, so as not to leave unaddressed needs.”

    Bit confused over the word ‘only’, since that infers that 1:60 is fewer than 1:110. Which it isn’t. 1:60 is approximately 0.01667 (4 s. f.), whereas 1:110 is approximately 0.009091 (again, 4 s. f.) ... and the ratio of the two is approximately 1.834 (yet again, 4 s. f.) – which is a significant difference.

    However, the inference regarding the difference could be correct, since almost twice as many children are getting the diagnosis than the overall national statistics figures would suggest. Where I used to live, the situation was – for a hell of a long time – quite the reverse of this: the diagnosis rate was practically zero. This wasn’t because there were actually no autistic children in that borough… it was because they had been avoiding diagnosing us!


  29. MJC
    January 4th, 2010
    20:21:31

    I agree that socioeconomic factors may play a role in the failure to diagnose clusters of disadvantaged children. However, it may go beyond simple diagnoses. Recent research is beginning to identify prenatal folate supplementation as a risk factor for autism spectrum disorders.

    Simply, folate supplementation allow embryos with deficiencies in folate metabolism to survive (they would have normally miscarried). These embryos develop, and are born. Once born, folate supplementation stops, and brain development is hindered. It just so happens that many individuals with autism spectrum disorders have an increased rate of mutations with genes involved in folate synthesis. Is it possible that affluent parents also have more access to prenatal vitamins? Lack of diagnosis of disadvantaged children plus an “environmental” factor such as enhanced folate supplementation of affluent parents could account for the clusters observed in the study.

  30. Hi MJC -

    Is it possible that affluent parents also have more access to prenatal vitamins? Lack of diagnosis of disadvantaged children plus an “environmental” factor such as enhanced folate supplementation of affluent parents could account for the clusters observed in the study.

    I had precisely this thought today. My wife was getting an ultrasound; her technician was a hispanic. We were talking and she mentioned that ‘hispanics just don’t get prenatal care as frequently’. It likely also means they aren’t getting lots of folate during pregnancy. It occurred to my wife a while ago that this was a big experiment; no doubt it has stopped spina bifida; but once the spinal column is formed, which happens relatively early in pregnancy, what are the effects of all this extra folate? We don’t know.

    – pD

  31. Passionless Drone, (and others)

    You are at it again, confusing incidence of diagnosis for prevalence.

    The rate of autism has not increased, nor is it I suspect different between Hispanics and Whites.

    Autism is around the same prevelance as it always has been, and what is different is when, and whether it is diagnosed.

    Hasn’t anybody got that yet.

    We simply do not have this argument in the UK, it’s a non issue.


  32. MJC
    January 5th, 2010
    20:56:02

    Laurentius Rex,

    I don’t know where you get your certainty from. Autism researchers as a group certainly don’t have it. While I believe an increase in diagnoses has bumped the total number of autism cases over the past two decades, a quick read through the scientific literature shows that many qualified and respected researchers are pursuing environmental hypotheses regarding the rise in autism rates (folate supplementation being one of them). As is true in most controversial fields, one answer is hardly the only answer. There is always room for additional research into possible environmental factors. Do we just throw our hands up in the air and stop asking questions? That is not how science works.


  33. MJC
    January 5th, 2010
    21:06:35

    There is a simple way to solve the dispute. Perform. the. experiment. Were the disadvantaged mothers in California taking an equal amount of prenatal folate as their affluent neighbors? If so, case closed. If not, there is still a question mark…

  34. Hi Laurentis Rex –
    While I can understand that you seem to relish your position of someone who thinks they know better than everyone and anyone else who researches autism, this seems a bit at odds with simultaneously being amazed that your statements are not being taken seriously.

    It is possible to acknowledge that autism is a condition with extremely diverse manifestations and indeed causes, with the understanding that our current tools for measurement have serious imprefections; they are still the best tools we have available. I, for one, am pleased that everyone has not thrown their hands up and proclaimed that this social construct is far too nebulously defined to be understood effectively. You are free to continue lobbying for this; funny enough, it serves my purposes quite well, to my mind. Keep it up!

    The fact that a discussion is had or not had in the UK is without utility in determining if it is an important discussion to be had or not.

    – pD

  35. Well yes I am certain, somebody has to be, and if I am wrong, then I am, but I am prepared to wait it out and see, and I don’t think I will be the one who is revising his opinions.

    What I do predict is that there will be a new group of putative causes and the ones being debated here will have been put to bed as surely as Bettelheim has been.

    You see what the scientists do is follow the money and there is a lot of money riding on causation, it takes dedication to pursue something you actually believe in, rather than continue an existing line of research simply because that is the only thing to do post doctoral. It is like everything social artefact.

    Someday somebody is going to discover something new and interesting, and probably quite unexpected too but not biomed.

    Its the unknown unknowns, all that is going on now is that there are so many rival road maps being printed, that is to say there is a vast amount of literature, but it will take time to see just how much of it is “noise”

    The problem still is with the definition of autism and the failure to understand it’s wider connections, the science needs to step back and broaden out somewhat, rather than effectively defining it’s own outcomes in circularity.

  36. Or to put it another way, it is like when all those crop circles appeared.

    On the one hand you have all the new agers and ufologists (the equivalent of the anti vax brigade) blethering on about extra terrestial causation, the new age of aquarias or whatever, whilst the scientists, deeply perturbed by this desperately try to come up with explanations that fit within the current science, freak vortices, electrically charged particles, I dunno.

    All the while a group of nocturnal ramblers are laughing in the pub with a plank and a bit of string beneath the table.

    The scientists are trying to explain something that probably doesn’t exist, they have made the fundemental mistake in following the notion that there is an increase in prevalence before it has been proven to exist. They have jumped the gun.


  37. MJC
    January 5th, 2010
    23:17:15

    “Well yes I am certain, somebody has to be, and if I am wrong, then I am, but I am prepared to wait it out and see, and I don’t think I will be the one who is revising his opinions”

    —I get the feeling that it isn’t the following hypothesis: the increase in autism rates is caused by more effective diagnoses, that you are trying to prove – rather your superhuman ability to foresee the future…

    “What I do predict is that there will be a new group of putative causes and the ones being debated here will have been put to bed as surely as Bettelheim has been”

    —Yeah, that’s how science works… You create a hypothesis, try to disprove it, and, if necessary, move on to a new hypothesis. Very insightful “prediction”.

    “You see what the scientists do is follow the money and there is a lot of money riding on causation, it takes dedication to pursue something you actually believe in, rather than continue an existing line of research simply because that is the only thing to do post doctoral. It is like everything social artefact”

    —Scientists have a lot more creative control of the experiments they perform than you think. Do they have to write grants to get the money? Yes. Once they receive the money, however, they can perform risky experiments that the scientific community wouldn’t necessarily agree with. Do you really believe that all of the scientific advances over the last 100 years were detached from government funding? The structure of DNA? The development of the smallpox vaccine? The poliovirus vaccine? Artificial limbs and organs? Surgical and chemotherapeutic techniques to cure some forms of cancer? The entire human genetic code? You can thank the American taxpayer and the NIH

    “Someday somebody is going to discover something new and interesting, and probably quite unexpected too but not biomed”

    —Are you kidding me? New and interesting things are discovered each day. Have you ever read a science journal in your life? Not biomed? What the heck do you even mean? Three-dimensional structures of viruses, human proteins, bacterial components, etc. are crystallized and solved each day. This data is new, interesting, and is changing the world as we know it. You can thank “biomed” for that! Why would the autism field be any different?

    —I have to admit, I’m a molecular virologist who works from cash given through NIH grants. While I don’t specifically work on autism, I am insulted that anyone would write off the professional scientists in that field. For what gain? No scientist ever gained anything by sticking to a specific hypothesis—refusing to engage in an open and objective debate. Maybe that is the issue at hand. Perhaps Laurentius (and others) aren’t trained scientists. If true, why would Laurentius spend so much time on an autism blog? Rather than respectfully being a part of the dialog, it seems that Laurentius has an agenda to push. If not true, I doubt Laurentius’ scientific career has progressed much…

  38. Of course I have an agenda to push, it is a disability rights agenda, an agenda to be treated ethically and respectfully by medical science, something that does not happen a great deal.

    In this country the usual way into a academic research career is to compete for funding from the appropriate board, usually on research topics already set by the University, unless one can bring ones own funds into it.

    I have already stated somewhere I am sure that my field is educational research, now methodology is just as important, the rules are the same, but the experiments are not. On the way one learns of the impact of sociology and social psychology on the workings of the researcher, nobody is free from pressures or influences of some sort.

    Whether or not I can predict the future is neither here nor there, what I do, like anybody else is watch trends.

    The point to be taken is that for a long time in the UK and elsewhere in Europe, it has pretty much been accepted that the autism rate is much higher than has been orthodox thinking in the US. Indeed a start (albeit an uncertain one) has been made on adult epidemiology.

    If it is established, as I am expecting it will be going by past trends, the work of Wing and Gillberg for instance, that the rate of autism amongst adults is as great, or very close as makes no difference within a reasonable margin of error, I am afraid all this search for new causational factors will be seen to be a little ridiculous.

    If there is an environmental factor, something I don’t rule out, I think it will be found to be something that has been around a very long time.

    I have a hunch, that is where we all start, that hunch becomes a hypothesis, and if one cannot disprove it, it remains more likely to be true than not.

    This is a testable hypothesis but the funding to test it is not as forthcoming as it ought to be, that is a political and a social factor.

    I do happen to know, from political circles that the funding for adult epidemiology was botched when the UK government made it’s committment, and what has appeared so far is but a pilot.


  39. dr treg
    January 6th, 2010
    00:30:33

    “If it is established, as I am expecting it will be going by past trends, the work of Wing and Gillberg for instance, that the rate of autism amongst adults is as great, or very close as makes no difference within a reasonable margin of error, I am afraid all this search for new causational factors will be seen to be a little ridiculous.

    If there is an environmental factor, something I don’t rule out, I think it will be found to be something that has been around a very long time.

    I have a hunch, that is where we all start, that hunch becomes a hypothesis, and if one cannot disprove it, it remains more likely to be true than not.

    This is a testable hypothesis but the funding to test it is not as forthcoming as it ought to be, that is a political and a social factor.

    I do happen to know, from political circles that the funding for adult epidemiology was botched when the UK government made it’s committment, and what has appeared so far is but a pilot.”

    Thank you so much for your erudite views Rex.

  40. There is a simple way to solve the dispute. Perform. the. experiment. Were the disadvantaged mothers in California taking an equal amount of prenatal folate as their affluent neighbors? If so, case closed. If not, there is still a question mark

    I am not surprised that you picked something which raises a question mark, by your own definition.

    In a recent study in Texas “Folic acid awareness and supplementation among Texas women of childbearing age”, they found that during pregnancy about 40% of non-Hispanic White mothers took daily folate. By comparison, about 24% of Hispanics did so.

    Does this really tell us something?

    Here’s a better question—do people of any ethnicity use prenatal supplements more than those outside of a cluster?

    There are a million or more such questions that can be posed. I hope that the epidemiologists are spending the time to ask smart questions rather than taking a simple Edisonian approach.

    People who actively advocate for environmental causation research need to take this study seriously. If there are environmental causes to be found it isn’t going to happen without knowing and controlling for factors like education and access to services.

    If they are sincere in their advocacy, they should welcome studies like this and Bearman and King’s recent study.


  41. MJC
    January 7th, 2010
    15:35:16

    “There are a million or more such questions that can be posed. I hope that the epidemiologists are spending the time to ask smart questions rather than taking a simple Edisonian approach”

    Edisonian approach? There are plenty of well-respected studies which support folate as a contributing factor to autism. Autistic individuals are more likely to have defects in genes related to folate metabolism for instance… Folate has also been shown to epigenetically modify the embryo. I don’t know if you can call a hypothesis with such support from the current literature Edisonian. With such support, what makes the “folate hypothesis” less smart than another?

  42. Hi MJC & Sullivan –
    It occurs to me that maybe the CHARGE or MARBLES studies currently underway could give us some insight into this. If I understand correctly, they are gathering markers from mothers and children from families that already have a child with autism. Perhaps maternal folate levels are included in that list of values being analyzed for.

    – pD

  43. It’s the same as the rise of diagnoses, isn’t it? It’s like an instinctive reaction. People think “if there are clusters made up of wealthy people, what is it that the wealthy people are doing to create autism?”

    Thinking like that probably leads nowhere but dead ends, unfortunately. Hypotheses based on that sort of idea can’t explain certain key observations, e.g. why is the prevalence of ASD in a semi-urban location of Sri Lanka over 1%? (When it was probably zero before any autism screening was done there.)

    To demonstrate that autism is actually associated with affluence, you can’t just select groups of diagnosed autistics. I’m getting a little tired of pointing this out, actually. You have to find all autistics in a population, diagnosed and undiagnosed, and then check for levels of affluence or anything else.

  44. Hi friends –
    I got an email from the MARBLES team this afternoon; maternal folate levels are being taken into consideration but it will be a few years before enough data, and presumably age appropriate children will be available for analysis.

    – pD

  45. Hi Joseph –

    Thinking like that probably leads nowhere but dead ends, unfortunately. Hypotheses based on that sort of idea can’t explain certain key observations, e.g. why is the prevalence of ASD in a semi-urban location of Sri Lanka over 1%? (When it was probably zero before any autism screening was done there.)

    I’d be curious on your take of the Faroe Island study, wherein every child in school was evaluated and a prevalance of .56% was found.

    http://www.springerlink.com/co.....u364g5255/

    This study got thrown around a lot when the mercury hypothesis was in vouge, but I don’t recall anyone pushing Wing as evidence that their methods were flawed because they must be missing one half of the people on the spectrum. I haven’t read the study, just the abstract; how did their sample size compare to the four diasgnosed children in the Sri Lanka study?

    But thinking about the tools in Sri Lanka gives me pause as towards if we should consider this a key observation or not. They only identified four kids with autism, and all were aged two or less. If one of them lost their diagnosis over time, something that gets bandied about when expedient, our prevalance in Sri Lanka plumets to ~ .75%. Aren’t we subject to large jumps in conclusions based on very small absolute changes with samples this size? On the other hand, however, if we want things to match up with Baron Cohens findings in adults, even a single loss of diagnosis hurts quite a bit.

    – pD

  46. This social class association is very un-new. See my discussion of the stark social class bimodal distributions already found 40 years ago, in my 1993-published paper linked at top of my blog. That was before the autism increase, and this report now is after it. So even after this supposed explosion of awareness, the level of unawareness remains in place? That seemingly does not make sense. Conclusion:—as I had concluded decades ago—autism is partly mainly genetic and partly mainly environmental.

  47. Startlingly not news, Robin. Never mind autism there is an association between socio-economic class and just about any medical condition you care to mention, going back to the Black Death in the 14th century and I dare say even further to whatever it was used to bother the ancient egyptians, pyramid builders back maybe.

    All the same you only have it two thirds right, part genetic, part environmental and a very big part socially constructed.

    Put it all together and it is all inevitable anyway including the responses to it.

    We not only, only see what we look for we only see what we want to look for and I bet Donald Rumsfeld wished he had said that :)

  48. “Any medical condition you care to mention….”. Indeed, but isn’t it usually biased towards the lower classes? The only other upper-class illnesses I know of are manic-depressive, gout (in historical connection to meat-eating), and caviar allergy. Oh, and allegedly dyslexia.


  49. RAJ
    January 13th, 2010
    19:38:48

    Laurentius Rex wrote:
    ‘One is essentially looking at the genetics of Unicorns”.

    Great quote, can I use it? In line with your observation, Moss and Howlin recently revisitd the genetic syndromes and ASD and found that the genetic syndromes have distinct and meaningful differences beyond ‘Autism’ and provided good evidence that the association between the genetic syndromes and ‘autism’ is superficial and related to the degree of cognitive impairment. Cognitively impaired people share one or another symptom with ‘true’ autism and researchers have never been able to control for cognitive impairment in the genetic syndromes.

    Take way the single gene disorders (Tuberous Sclerosis, Fragile X, Angelman’s Syndrome, 16P mutation, Rhetts Syndrome, Downs Syndrome etc. ) and all that the researchers are left with is ‘One is essentially looking at the genetics of Unicorns”.

    http://www.ncbi.nlm.nih.gov/pubmed/19708861?


  50. meester
    January 14th, 2010
    18:15:40

    Not to minimize specific examples of helping specific people but this is another good example of the broader problems created by supporters of and the current leadership in the Congress, Senate and Presidency. The more things are done to “help the poor” the more “poor” is perpetuated. More help is available when a broader base of success is prevalent in the country and more people will benefit. When people are more free they are more successful and more people benefit broadly.
    Besides doing specific things please consider the broader concept as well so more of us can help or benefit.

  51. This is beginning to get a bit political.

    I think what you find is that the more the rich help themselves the more “poor” is perpetuated.

    Wealth does not trickle downwards, it pools in the rich districts and creates ever increasing barriers for people in poor neighbourhoods.


  52. Tom
    January 19th, 2010
    00:23:16

    Look at EEG’s of infants who sleep on their backs compared to infants that sleep on their stomachs. Something as simple as a change in sleep position causes huge physiological changes. But, just because it’s not a drug or a pollutant or “genetics” it isn’t analyzed as a possible cause of autism.

    If a known vaccine or pollutant caused an increase in sleep apnea, lowered subcortical arousal thresholds, obliterated Stage 3 NREM sleep, obliterated stage 4 NREM sleep, increased the number of infant arousals, and was also shown to cause increases in plagiocephaly, torticollis, hip subluxation, and strabismus there would be people screaming in the streets. But, since the back sleep recommendations are mandated by the medical community it’s ok. Just like thalidomide the long-term implications of the back to sleep campaign have never been analzyed. Never. People in Asia have put their infants to sleep on their backs for generations but that is a “cultural practice” which is far different than a medical recommendation. Just food for thought.


  53. Chris
    January 19th, 2010
    01:34:01

    Tom:

    Just like thalidomide the long-term implications of the back to sleep campaign have never been analzyed.

    Can you tell us when thalidomide was approved in the USA for children or pregnant women? I was under the impression that it was not approved for use in the USA because the European company did not provide the requested data.

    As far as the “back to sleep” program, it was a recommendation, not a mandate. You should provide evidence for your assertions of the harm. If you worry about the shape of a baby’s head, then pick the child up and cuddle. Let the child have some tummy time. It sounds like you are making a mountain out of a mole hill.

  54. Hello friends –
    One of my pubmed alerts recently sent me this terrifying link, Body burdens of brominated flame retardants and other persistent organo-halogenated compounds and their descriptors in US girls, which may have some interesting information for this type of discussion. In it, researchers describe very different levels of a variety of endocrine disruptors and pesticides over geographical area, race, cultural practices, and BMI in US female children.

    Ethnically diverse cohorts of girls 6–8 y old at baseline are being followed for growth and pubertal development in a multi-site, longitudinal study. Nearly 600 serum samples from the California and Ohio sites were analyzed for lipids, 35 PCB congeners, 11 PBDE congeners, and 9 OCPs. The biomarker distributions were examined and geometric means compared for selected analytes across categories of age, race, site, body mass index (BMI), parental education, maternal age at delivery, and breast feeding in adjusted models. Six PBDE congeners were detected among greater than 70% of samples, with BDE-47 having the highest concentration (median 42.2, range 4.9–855 ng/g lipid). Girls in California had adjusted geometric mean (GM) PBDE levels significantly higher than girls in Ohio. Furthermore, Blacks had significantly higher adjusted GMs of all six PBDE congeners than Whites, and Hispanics had intermediate values. GMs tended to be lower among more obese girls, while other variables were not strongly associated. In contrast, GMs of the six PCB congeners most frequently detected were significantly lower among Blacks and Hispanics than Whites. PCBs and the three pesticides most frequently detected were also consistently lower among girls with high BMI, who were not breast-fed, whose mothers were younger, or whose care-givers (usually parents) were less educated. Girls in California had higher GMs than in Ohio for the pesticides and most PCB congeners, but the opposite for CB-99 and -118.

    The paper goes on to speculate that some of these findings may be driven by more robust regulations in fire safety in California.

    These findings struck me as a bit counter intuitive; we usually think about environmental exposures as operating over very large areas that do not discriminate by things like race or education, and yet, here we observe the opposite. Considering we have several disparate studies involving a variety of endocrine disruptors or pesticides pointing to a link to autism, I’m not sure that it is safe to assume that diagnostic availability is the sole driver for different rates of autism.

    – pD

  55. Passionless you are chasing after Unicorns again. Your presumption that there MUST be an environmental cause is causing you to find that in cases where it is the data that are dodgy in themselves, e.g. the CDC statistics that contain enormous socio-economic artefacts. You are in effect looking at the data and failing to see the obvious because you have a passion for seeing something else.

    Let us suppose for example that a victorian police inspector becomes interested in the phenomenon of “Bertillonage” the now discredited ‘science’ of relating an individuals phsyiognomy to his criminal propensity.

    If he were a true believer this inspector might find himself seeing the evidence of criminal physiognomy in his colleagues on the police force, which provokes him then to start investigating each an every one of them on the basis that they must have committed some crime in order to rid the force of ‘bad apples’

    That may be a hypothetical example but unfortunately similar misplaced faith in ones scientific truth has led to miscarriages of justice in the case of cot deaths, not to mention those who see Munchausens everywhere or evidence of Satanic abuse.

    These people eventually become lost to science or reason, and usually end up fielding the Galileo gambit.

  56. LRex, I agree that the Galileo gambit is a fallacy. But you should beware of an actually more insidious fallacy, which we could call the inverted Galileo gambit. It is very frequently deployed and goes like this: “This work is being ignored and or “debunked”/disproven/despised by all the experts; therefore it is reasonable to dismiss it as unsound”.

    To understand the reality you have to bear in mind that the vast majority of “great discoveries” are unsound, with just a tiny minority of sound ones. It follows that the vast majority of Galileo-invokers, or even just despised ideas, are unsound, and yet it does not follow that most sound ideas are promptly recognised. Instead there’s a wealth of evidence that the greatest breakthroughs regularly encounter great hostility, see http://www.autismcauses.info/2.....tific.html. Galileo seems to be indeed the rule rather than the exception.

  57. Hi Laurentix Rex –
    It occurred to me that the irony is that our viewpoints seem to share a similar foundation; the difficult to understate stupidity of humans. To you, this is a reason that we have not begun yet to understand autism, and consequently, our observations are so tainted, we cannot reach any conclusions from them. [at least, I believe this is part of your view.] On the other hand, my view is that we have introduced synthetic chemicals into our environment with such recklessness, we cannot help but have had impacts; especially considering how nascent our understanding of how many of these chemicals interact with our own bodies machinery.

    As far as CDC statistics go and the problems with data fuzziness, the study I posted about is following specific children whose parents answered questions like: ‘Is the child white, blank, or of hispanic?’ or, ‘How many months did you breastfeed?’ or ‘How old were you when the child was born?’. This data is not subject to the problems you would ascribe to it.

    While your parable is eloquent, unfortunately, it does nothing to change the repeated clinical findings of deleterious effects of many of these types of chemicals to the developing nervous system. This type of study isn’t being funded and conducted by rationale of eighteenth century theory, but rather, after dozens or hundreds of studies showing that these molecules can interrupt, or augment, critical metabolic processes. If you would like to paint the science of endocrine disruption as soon to be discredited, you will have to bring a stronger case than trotting out “Bertillonage” and imperfections in statistical models.

    – pD

  58. Well I chose Bertillonage because I wanted an example of something that had been completely discredited rather than something which is still disputed by a minority, for instance the notions of racial differences in g.

    However there is another logical fallacy committed by the self proclaiment anti neurodiversionists and that is to assume that because I do not believe that x, y or z causes autism, that I believe that x, y or z is necessarily a good thing.

    I dare say there are lots of background effects from toxic chemicals in the environment, however they are not significant enough to cause the rather specific (however ill defined at the edges) phenomenon of autism. PCB’s organophosphates and heavy metals are there but I think they pale into insignificance with the amount of gunk one introduces into the system when on smokes a cigarette and if anything were around that could have affected my development in the womb smoking would be it. (not that I am saying it is)

    Pure genetic arguments won’t wash, neither will pure environmental ones, there has to be some threshold of genetic complexity that maybe triggers specific susceptibilities that then encounter a sort of multiplier effect, you know the equivalent of the butterfly effect in the chaos mathematics of the weather system.

    The problem too with a lot of this looking for new causes for autism is the assumption that is is increasing, which I do not buy, if it is toxins you are looking for, something that has an effect prenatally, there is plenty that has been around since before PCB’s

  59. Laurence, I liked your thing about the “persons with autism” nonsense (in concurrence with my http://www.autismcauses.info/s.....orrectness ).

    Meanwhile you reckon/suspect that autism is not increasing. I’d be interested to know what you think is most likely going on in this second graph here: http://www.autismcauses.info/2.....graph.html. Cheers.

  60. LRex, I liked your thing on the “persons with autism” nonsense, in line with my own http://www.autismcauses.info/2.....about.html.

    Meanwhile you reckon/suspect that autism has not been increasing. In view of that I’d be interested to know what you think is the most likely explanation of the second graph here: http://www.autismcauses.info/2.....graph.html. Cheers.

  61. Hi Laurentis Rex –

    However there is another logical fallacy committed by the self proclaiment anti neurodiversionists and that is to assume that because I do not believe that x, y or z causes autism, that I believe that x, y or z is necessarily a good thing.

    Well, I’m trying very hard lately not to assign arguments to people they do not make. My line of reasoning allows for improved diagnostics and the like to be impacting our observations, but the notion of a static rate of autism allows for no environmental impacts; your argument that there is no real increase in autism implies a non impact of these types of chemicals. A good thing versus a bad thing is difficult to assign here.

    I dare say there are lots of background effects from toxic chemicals in the environment, however they are not significant enough to cause the rather specific (however ill defined at the edges) phenomenon of autism.

    Well, this gets murky pretty quickly, as part of your argument (I think), is that we can’t even quantify autism sufficiently.

    However, what we are finding is that these chemicals are capable of causing neurological differences and/or interferring with metabolic processes that we already have associated with autism, or other neurological conditions.

    For example, hypothyroidism is associated with autism, again in autism, and impaired intelligence and motor skills and more. We have a good body of evidence on the importance of thyroid metabolism in brain development. It turns out, we also have detailed information on how some of these environmental pollutants can modify thyroid metabolism, and indeed, affect the developing brain.

    For example, here, here, here, or here.
    Or, we can look to this study that found associations between PFOA levels and thyroid problems. Or many, many others. The fact that people have smoked during pregnancy for some time does absolutely nothing to change these findings.

    Pure genetic arguments won’t wash, neither will pure environmental ones, there has to be some threshold of genetic complexity that maybe triggers specific susceptibilities that then encounter a sort of multiplier effect, you know the equivalent of the butterfly effect in the chaos mathematics of the weather system.

    I have no problem with very complicated genetic and environmental interactions, but I’m not sure that it necessarily involves application of chaos level theory.

    The problem too with a lot of this looking for new causes for autism is the assumption that is is increasing, which I do not buy, if it is toxins you are looking for, something that has an effect prenatally, there is plenty that has been around since before PCB’s

    Speaking of fallacies, using the fact that because there have been mechanisms by which the prenatal environment could be affected for a long time, that therefore, our newly minted forces must not be having a significant impact is a whooper. By way of example, examination of smoking and altered thyroid hormone levels was recently found in NHANES data in Cigarette smoking and iodine as hypothyroxinemic stressors in U.S. women of childbearing age: a NHANES III analysis. Smoking levels may have decreased somewhat over time, but when your mother was of child bearing age, a great many of our current suite of sythentic chemicals hadn’t been invented, much less distributed widely.

    – pD

  62. pD, A commendable job of links to associations there. You could have added that hypothyroid is a significant consequence of adult amalgam poisoning (as if I need reminding myself, 35.9 this morning, with world record oral Hg vapor of 460mcg/m3).

    However the problem with these sorts of association is that it soon gets to feel like just about everything is associated with everything else. In the absence of Mengeleian interventionist experiments or any “outside” pointers to the directions of the causality arrows, some very boring books could easily be written consisting entirely of speculations about how those arrows might link together into nice diagrams. (Actually, come to think of it, one such boring book may have already been written in Cambridge uk!)

    A way out of this insoluble maze could be to look at other evidence, such as the nature of the symptom syndrome, as for instance I did in my own explanation. I asked the question of quite what the autism characteristics have in common. Answer: they are suppressions of innate programmings/tendencies. But then the handflapping, webbed feet etc contradicted that. To address that we add in the established concept of reversions to atavisms, which enables the handflapping and other peculiar things to be explained with due Occam’s Razor principle.

    Such an analysis does not result in anything like total clarity about everything about autism. But I would argue that it allows a start on climbing out from that boring books quagmire.

  63. Hi Robin P. Clarke –

    . In the absence of Mengeleian interventionist experiments or any “outside” pointers to the directions of the causality arrows, some very boring books could easily be written consisting entirely of speculations about how those arrows might link together into nice diagrams.

    Hm. Well, have you read this study, Associations between indoor environmental factors and parental-reported autistic spectrum disorders in children 6-8 years of age, where researchers report a rough doubling of autism risk if raised in home with PVC flooring? [as does a smoking mother]

    One of the links I sent indicated changes to the brain in very specific areas associated with autism by many studies, purkinje cells, Disrupting effects of hydroxy-polychlorinated biphenyl (PCB) congeners on neuronal development of cerebellar Purkinje cells: a possible causal factor for developmental brain disorders?

    Did you know that children with autism have been found to have reduced levels of molecules used in detoxification of organic pesticides? Paraoxonase 1 activities and polymorphisms in autism spectrum disorders

    The direction of these arrows seems pretty straightforward to me, but may be boring to some. (?)

    Such an analysis does not result in anything like total clarity about everything about autism. But I would argue that it allows a start on climbing out from that boring books quagmire.

    Maybe. (?) Unfortunately, I’m not sure I understand your position clearly enough to say for myself.

    – pD

  64. Hm. Well, have you read this study, Associations between indoor environmental factors and parental-reported autistic spectrum disorders in children 6-8 years of age, where researchers report a rough doubling of autism risk if raised in home with PVC flooring? [as does a smoking mother]

    That sounds a lot like data dredging, and reminds me a bit of Dr H-P’s pet shampoo finding. Even if they did control for multiple comparisons, it’s prudent to wait for an independent replication to start to believe it’s possibly true.

  65. Farbeit from me to interrude between Joseph and pD here, but,
    I think J’s point about data dredging is far from entirely unsound, and is part of the reason why I think one should not get too unbored by such reports, when untethered from any wider theoretical moorings.

    But I think nevertheless I got overdone with my ‘boredom’ there. The first and last look like worthy studies. I’d put them alongside the evidence about Lyme disease being autism-associated too. (It soon starts to look like everything causes autism doesnt it?!)

    I’d then tie all these envirofactors in with my mercury-caused-increase updated concept, as follows. They all, I hypothesise, as nasty toxins, stress certain detox capabilities and thus tend to throw the system into a detox failure (such as is hypothesised by those DAMN! people). Thereby these organic nasties make the victim more vulnerable to the effects of the increasing dental mercury onslaught. So everything (at a rough approximation) adds up. Someone with more time and energy (and months of ‘life’ left) could do a great job of precisely calculating the exact factor analysis of it all.

    As for the directions of the arrows, some higher class parents might prefer the latest Swedish fashionable gimmick of PVC in their bedrooms and the higher autism be caused by their genetics alone with no causality from the pvc. Or such like. Until you have an anchoring theory and a good knowledge of the context, anything goes.

    As for the pcbs zapping the Purkinjes, lots of things zap lots of things, and it doesn’t necessarily follow that the pcbs cause any significant level of autism. They might merely damage the Purkinjes specifically and this tend to spuriously inflate autism diagnoses. I’d compare this with the famous youtube of mercury decomposing a neuron with allegedly great similarity to Alzheimers; again I’m sceptical of this as “proof” that mercury is a main cause of AD by that mechanism or anyhow.

    (pD: Re understanding my position, it is that everyone else is partly wrong. More precisely, there is firstly my 1993-published paper. To which is now added a draft of an update review paper. The latter is not puttable on web until accepted by a journal, but can be got by emailing a request to rpclarke[at]autismcauses[dot]info, cheers.)

  66. More on the PVC in bedrooms. The idea of having PVC in one’s bedroom strikes me as distinctly weird/nutty. It suggests living in a relatively quiet, wealthy neighbourhood. But one still has to wonder quite why anyone would choose PVC for their bedroom. Apart from the nut factor (which could genetically link to autistic descendants) there could be a concern for reducing allergen/pollutant exposure. So the choice of PVC could also be a consequence of the parents’ difficulty with allergy/immune/detox. And thereby a genetic connection again with no causation by the polymer.

  67. Hi Joseph –

    That sounds a lot like data dredging, and reminds me a bit of Dr H-P’s pet shampoo finding. Even if they did control for multiple comparisons, it’s prudent to wait for an independent replication to start to believe it’s possibly true.

    According to the author, this was supposed to be a studyregarding asthma, but the numbers of children with autism that were correlated to vinyl flooring were so significant that it warranted publication.

    http://www.scientificamerican......-and-vinyl

    I don’t know if that is data dredging or not. (?)

    The authors make a similar call for caution and additional study before any conclusions can be reached.

    – pD

  68. Hi Robin P. Clarke –

    As for the pcbs zapping the Purkinjes, lots of things zap lots of things, and it doesn’t necessarily follow that the pcbs cause any significant level of autism.

    Well, Purkinjes do seem to be particularly vulnerable to a variety of insults, however, I’m curious if you are aware that deficiencies of Purkinje cells are among the most widely observed neuroanatomical difference observed in autism? I don’t want to earn another commendation on link spamming, so I’ll leave that research up to you, but even with everyone being wrong somewhat, it is difficult to paint a scenario where Purkinje cell development (or abnormal development) is involved with at least a subset of autism cases.

    Re understanding my position, it is that everyone else is partly wrong.

    This sounds a lot like my ideas, to tell the truth.

    Finally, the flooring in the mentioned study was vinyl, something not so exocit as pvc piping as floors. I believe the salient idea is the breakdown of the materials.

    – pD

  69. Vinyl is the popular word for PVC. And it’s 4am over here in the civilised world so g’nite.

  70. The Purkinje abnormalities just happen to be big (they are after all big cells involved in big movement stuff). Most of the behavioural syndrome is very unlikely to be attributable to them, just the other abnorms are subtle tweaks in the undercomprehended info-tangle in front of the cerebellum.

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