passionless Droning about autism

My original intention on starting this blog was to try to create more comprehensive, wide ranging screeds on autism than you might usually see in the blogosphere.  Alas, this has seemed more difficult and time consuming that I was hoping it might, and my posts have been small.  It was suggested to me by Kev at Left Brain / Right Brain that I ‘get my own blog’ if I didn’t like what he was interested in.    While I’m not exactly taking his advice, it did occur to me that the post I intended to write back in response to a couple of posts there was lengthy enough and had thoughts I wanted to have stored more accessible that I could go ahead and double post it. 

The thread on  LBRB is here, wherein I mentioned that familial commonalities may not necessarily be the result of genetics per se, and was consequently challenged by dueling interpretations of the twin study fallacy.  Here was my response:

Hello friends –

I’m not here to deny a genetic component to autism, but the lightning fast gunslinging of twin studies hinges on the notion that there is only one way to get to a particular developmental endpoint – genes. If we accept that there are other ways to achieve a particular developmental endpoint, a reliance on twin studies shows itself as a fallacy. You can have genetic and environmental mechanisms affecting neurodevelopment if we allow ourselves to believe that autism rates are increasing, but you can’t have the opposite; to believe that autism rates are stable, completely stable, we can’t allow any intrusion of changes to our environment to be affecting neurodevelopment.

Of course, when pressed, say with studies involving something like valporic acid, as mentioned by Socrates, and a whopping increased risk, you can get the acknowledgement that there are some things that can cause autism that aren’t genes, quickly followed by the impossible to substantiate claim that the amount of increase is very minor.

Unfortunately, we need to start ignoring mounting reams of clinical evidence from a galaxy of sythentic chemicals for this to make any sense.

Take the study I posted above, Prenatal Exposure to Organohalogens, Including Brominated Flame Retardants, Influences Motor, Cognitive, and Behavioral Performance at School Age, which, curiously, got left out of any discussions so that we could discuss twin studies.   To illucidate briefly the frailty of an argument exhonnerating our influx of chemicals into the environment, lets examine one of the proposed mechanisms by which organohalogens are believed to affect neurodevelopment; affecting thyroid metabolism.

OHCs are known to exert their neurotoxic influence by affecting thyroid hormone homeostasis. It is hypothesized that OHCs affect thyroid hormone homeostasis by interfering with thyroid hormone signaling in the developing brain, by changing intracellular thyroid hormone availability, and by interacting directly at the level of the thyroid hormone receptors. On the one hand, OHCs have a high affinity for thyroid hormone receptors and lead to a decrease in thyroid hormone levels, whereas levels of TSH increase through hormonal feedback mechanisms. Previous studies on pregnant women and their infants found that PCBs are associated with higher levels of TSH and lower levels of T4 (Koopman-Esseboom et al. 1994). We found that PCP correlated with lower levels of thyroid hormone but brominated flame retardants correlated with higher levels of thyroid hormone. It is unknown whether the underlying mechanism by which PCBs affect thyroid hormones is the same for these OHCs. Our study disclosed consistent relations between thyroid hormones and outcome. We found that TSH correlated with worse neuropsychological functions. Thyroid hormones (T3 and T4), by contrast, correlated with better outcome. These findings, together with the negative correlations between OHCs and development, seem to confirm the hypothesis that thyroid hormone homeostasis may be involved.

There are a number of studies showing the ability of a wide range of chemicals to modify thyroid metabolism, here, here , or  here. 

 Having thyroid metabolism interferred with during pregnancy is associated with a variety of bad outcomes, inclding, Pervasive developmental disorders, autism, reduced cognitive abilities , ADHD  and many, many other condtions.

 Unsurprizingly, when we look for associations between levels of these chemicals and development outcomes, we find results that should surprise no one, such as the study I linked to above, or another, here. 

The facts on the ground are that these chemicals are completely novel to our planet in the past few decade and many have reached environmental ubiquity. We have a growing understanding of the mechanism(s) by which these chemicals can affect developing brains, and association studies that indicate that our clinical observations have merit for a variety of conditions, including autism.  Finally, we seem to be observing an explosion of ever increasing behavior patterns that no one can really explain without necessarily invoking an the ever hopeful idea of progressing decrease in uncertainty of our diagnostic as rates continue to go in a single direction. The fact that twins have autism more frequently does absolutely nothing to change any of this if we allow ourselves to believe our observances of increase are not completely an artifact; but the inverse does not hold true. We must find a reason to believe that all of these studies, and many, many others are all wrong in exactly the same way for our environmental engineering to be without consequence.

 – pD