passionless Droning about autism

Archive for the ‘The Fairytale’ Category

Hello friends –

Recently there have been a few studies that tackled the issue of apparent autism clusters in California, The spatial structure of autism in California, 1993-2001, and Geographic distribution of autism in California: A retrospective birth cohort analysis.   A nice overview and some discussion of these papers can be found at LBRB, here, and here.  One of the arguments we see made there is that the rates of autism diagnosis are, in fact, a reflection of the available services in an area, as opposed to an actual difference in the number of children with autism; essentially that an undiagnosed child with autism who lives far from a center of autism services will not get a diagnosis, but a child born relatively close to such services, will be appropriately diagnosed.  We are measuring diagnosis, as opposed to autism.  I have no doubt that there is some validity to this, but have many doubts that we can, or should, assign all of our observed increases in autism as consequences of this type of artifact. 

There have been several other studies that looked at things like mercury emissions, or airborne pollutants, or Superfund sites and autism rates at larger scales.  However, on a macro level, these types of studies have, so far, been unable to design around a feature of reality; the likelihood that things like Superfund sites or airborne pollution are situated in relative proximity to an urban center, and as such, autism diagnosis services.  In effect, the argument that these observations are diagnostic only is the same; without a controlling factor for diagnostic availability, we can not assume that other parameters are actually responsible.  And again, I have no doubt that this is a force that contributes to the findings of these studies.

But.

At the end of the day, I’m just not satisfied with a God of the Gaps explanation; what we seem to be seeing is just too goddamned important to explain away with the spongy soft and ultimately unmeasurable forces of greater awareness et all. (The Fairytale, 20##). 

Anyways, the other day pubmed alerted me to the publication of  this interesting study: 

 Body burdens of brominated flame retardants and other persistent organo-halogenated compounds and their descriptors in US girls.

BACKGROUND: Levels of brominated flame retardants are increasing in US populations, yet little data are available on body burdens of these and other persistent hormonally active agents (HAAs) in school-aged children. Exposures to such chemicals may affect a number of health outcomes related to development and reproductive function. OBJECTIVE: Determine the distribution of biomarkers of polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs), and organo-chlorinated pesticides (OCPs), such as DDT/DDE, in children, and their variation by key descriptor variables. METHODS: Ethnically diverse cohorts of girls 6-8y 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, 36 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. RESULTS: Six PBDE congeners were detected among greater than 70% of samples, with BDE-47 having the highest concentration (median 42.2, range 4.9-855ng/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. CONCLUSIONS: Several of these potential HAAs were detected in nearly all of these young girls, some at relatively high levels, with variation by geographic location and other demographic factors that may reflect exposure pathways. The higher PBDE levels in California likely reflect differences in fire regulation and safety codes, with potential policy implications.

The environmental impact argument usually focuses on vaccines, or in some instances, similarly widespread environmental pollutants (i.e., mercury emissions); external forces which tend to operate more or less evenly across large geographic swaths, and also largely independent of things like culture or race.  But with this paper we can observe the counter-intuitive opposite,  chemicals that have achieved widespread distribution in society and the environment, seem to be bioaccumulating differentially according to factors such as geography, race, body type, and education levels.  The paper here mentions fire regulation as a possible factor in state by state differences, but taking things a bit further, it can quickly be seen how socio-economic factors might play a role in why we might observe different levels of chemicals.  It takes a lot of crazy chemistry to make a baby onesie not catch on fire, but at a high level, it involves dousing the material with a bunch of exotic chemicals.  Politically correct or not the facts on the ground are that the well to do white woman has baby showers where she gets a bewildering array of freshly minted, ‘extra safe’ baby clothes more often than,  say, the not so well to do Latina woman.  We have already established a connection between having older parents and a diagnosis of autism, it would seem, there is also a correlation between having older parents and your bodies burden of these molecular mimics; and again, white women tend to have babies at later stages in life than their Black or Latina counterparts; especially the ones that happen to be residing near the trendy autism diagnosis hubs (i.e., the wealthier white women).    The ability for these types of chemicals to cause a variety of difficult to predict developmental trajectories is too long, and terrifying to go into detail in this post; for purposes of this discussion, it is sufficient to understand that we have a growing body of evidence that endocrine disrupting compounds can have wide ranging effects; including epigenetic changes, changes in immune profiles, altered behaviors and neuroanatomical structures known to be abnormal in autism

I found the finding of BDE-47 particularly intriguing, considering it was used as a primer for immunological response measurement by Ashwood, who found in vitro differences in immune responses in the autism population (an exaggerated innate immune response was observed).

Of course, this study does not present sufficient evidence for us to draw conclusions about the geographic distribution of autism rates in the two California studies above; but it should give us enough to pause before we take the comforting road out and assume that our observation are the result of diagnostic artifact alone; such assumptions feel good (except for the guilt), but ultimately require that we ignore our growing knowledge of how unpredictable endocrine disruptors affect the body, and how much more we have to learn.

– pD

Hello friends –

One of my biggest problems with the Fairytale of a Static Rate of Autism is that we need to ignore the reckless environmental engineering that our species has engaged upon in the past few decades.  My concerns lay within the inherent, difficult to underestimate stupidity of our actions, wherein our perceived understanding of the impact our actions are far less pronounced than the actual impact of our actions.   For the telescopic illustration of this worldview, go back any number of years where X is greater than thirty, and see if the expectations and predictions of those times match up well with what has actually occurred.     While our achievements are great and wondrous, it is at our great peril we come to believe we understand sufficiently our actions to predict their outcomes. 

In any case, a progenitor of great concern, or indeed, impending doom, to my mind, is the increasing environmental ubiquity of a variety of industrial chemicals that have the potential to interfere with biological processes in difficult to predict ways, endocrine disruptors.   Although there are no doubt naturally occurring substances with similar properties, for purposes of this discussion, lets assume that my concern (and yours), should be with chemicals that were manufactured by man that have molecular structures so similar to naturally occurring molecules that they can interfere with low level metabolic processes in a myriad of ways that are difficult to understand without very detailed analysis.  Unfortunately, subtle effects during critical developmental time frames can propagate outward into long lasting, not so subtle effects.  Doubling down, we are largely reliant on corporations largely responsible for the next quarter share price to ascertain if subtle effects are happening or not. 

To  start the horror show, considers Bisphenol-A , a plasticizer used in pretty much everything, but especially in things like the tupperware you put in the microwave, bottles you give your baby, canned goods, or anything else you buy in the grocery that has a shelf life.  This particular mish mash of atoms tends to break down into something that is chemically very similar to estrogen, so similar, in fact, that the keys and locks of the cellular machinery of your metabolism can get confused.   It turns out, when this happens, we start seeing disturbing associations between circulating levels of BPA and a variety of conditions you’d rather not have, including heart disease and diabetes.  On top of tons of animal models of BPA exposure and metabolic dysfunction, immune changes, and we now have several human studies wherein urinary levels of these chemicals is associated with adverse outcomes.    And those are just the direct effects!

It would seem that BPA can have epigenetic effects too, wherein it can modulate which genes get expressed, and that’s a lot like getting a whole different set of genes.  For a fascinating (and terrifying) ride, I’d recommend that anyone take a look at this slide show from NOVA science now that goes over some of the effects of BPA to a prenatal environment.  I  double dog dare anyone who doesn’t think we are doomed to watch this episode. 

That was the good news. 

The uncontested facts on the ground are that, as a species, we are being exposed to BPA in ways that no previous generations of humans, or mammals, vertebrates, invertebrates, or living thing has ever been exposed to.  There is no way we are clever enough to understand the ramifications of this, and yet, we have up and distributed BPA in measurable and non trivial concentrations in every human body touched by modern convenience. 

The Scary Chemicals stories will involve research on a variety of chemicals identified as endocrine disruptors with known or suspected properties that would allow them to interact with development in ways meaningful to autism research.   BPA is one.  There are many, many others.

Oh well.

– pD

Hello friends –

This post really ought to be Chapter 1, but since I wrote the other post first, and sort of liked the title, so  we’ll just pretend; these posts are all about make believe in any case, right?

There is only one valid reason not to vigorously pursue environmental causes of autism; you need to believe that our observation of an increased rate of autism, one hundred percent of it, is an artifact of the four horsemen of the imaginary increase:

  • Diagnostic Substitution
  • Greater Awareness
  • Increased Accessibility to Diagnosis
  • Widening of Diagnostic Criteria

Lets start off with a couple of honest admissions and the reason they don’t make a whit of difference if our goal is to expose the notion of a static rate of autism as a fairytale, and a dangerous one at that. 

  • I have read very few papers regarding prevalence fully.  In fact, I can’t think of the title of a single one.   In the context of a precautionary principle, however, the methods and discussion for this type of study don’t really matter much;  because the brush strokes used to craft the results are so necessarily broad and imprecise that they are admitted as meaningless even by people who believe in the fairytale.  Think about it.   The only way we have a static rate of autism is if all of our previous studies utilized methods of such poor quality that they missed ##-## per 100,000 cases of autism, where you get to replace ##-## with any set of numbers lower than 100 as you move backwards in time.  The conclusions in our previous prevalence studies are so discordant over time that the flaws in their methodology are the super strings of the fairytale; responsible for all of our observations of increased autism rates while having  natural physical properties that render them impossible to elucidate on completely.  Given that even the proponents of the fairytale don’t give the methods of previous studies any currency, why should anyone? 

 

  • I cannot provide meaningful estimates on what percentage of the observed increase in rates is real versus artifact.  Again, however, in the prism of a precautionary principle, it doesn’t matter, because any amount of real increase is alarming, and the only possible unalarming possibility is a zero percent increase.  Here is a little thought exercise to illustrate this; imagine you are on a debate team and the topic is; “Autism rates have risen by X percent, health crisis or not?” and your team has drawn the ‘not a crisis’ side.  Insert any number greater than zero for X, and then try to construct debate points to make this argument to a crowd of skeptics.  This argument is implied whenever the fairytale is invoked, sometimes with the assertion that any real increase is “minor”, but one surefire way to get a storyteller to dissolve from a discussion is to try to get a value more concrete than “minor”  for X.   Autism is a disability, and while there are arguments to be made that it is also a ‘difference’, it isn’t a difference like having red hair or being left handed anymore than dyslexia is a different way of reading; any true increase has broad implications for us all. 

 

  • I have no doubt that the four factors listed above are, indeed, responsible to one degree or another towards what we are observing in autism rates.   Unfortunately, unless we are able to explain our ever rising rates of autism completely with these explanations, we still must contend with ramifications of a true increase.  

Even with the above caveats, a compelling case can be made that what we are observing is comprised of an actual increase in behaviors consistent with an autism diagnosis,  and the argument that autism rates are static is long on faith and very low on the lifeblood of science; reliable data. 

– pD


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