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Saturday, May 5, 2012

Autism, Obesity and the Metabolic Syndrome

AUTISM.  No childhood condition is more complicated or less understood.  We're not even sure how to talk about it.  Is it a "condition" at all, or more like a symptom pointing to other underlying problems?  And if the latter, what kind of problems? And perhaps most vexing of all: Is the prevalence of autism increasing?  The is very good reason to believe that some of the apparent increase is the result of better detection among mildly affected children; reclassification, or what some call "diagnostic substitution" seems to be at work as well.  But is there more to the story? We don't know.

One thing is clear.  We will never understand autism until we understand its causes.  And such causes appear to be numerous and diverse. Researchers are reasonably certain that autism has a strong genetic basis, but that "environmental" factors play an important role as well.  Does this kind of thinking make sense?  Skeptics argue that this is just a lot of mumbling among scientists, and a sophisticated way of avoiding the difficult admission that we are in the dark.  Before tuberculosis was found to be the result of infection with a special bacterium, "experts" blamed it on multiple causes, like climate and crowded conditions.  

However, autism is probably more like cancer than tuberculosis.  Meaning that it simply isn't a single condition, but a whole host of conditions, with separate causation, prevention, symptoms, outlooks and treatments - hence the "spectrum."  And these conditions may have very different causes.  This isn't good news of course - its much easier to tackle a single condition than a "category" of disorders.  

In the May issue of PEDIATRICS,  a team from UC Davis and Vanderbilt University report on their evaluation of more than five hundred children on the autistic spectrum between 2 and 5 years of age, comparing them with 172 others with developmental disorders and 315 age-matched controls.  A major purpose of the study was to see whether the parents of affected children were any more likely to suffer from "metabolic" conditions, including obesity, diabetes and high blood pressure.  They were.  For families with a child on the spectrum, the odds of a mother having one of these conditions was 1.6 times higher than for a "control" family.  What does this mean?

On the one hand, a case-control study like this needs to be interpreted cautiously.  Did the mother's diabetes or obesity cause autism?  Or are these conditions all the result of the same common (genetic) factor?  Other kinds of investigation will be needed to confirm the association and better work out the matter of causation.  On the other hand, these results may turn out to be very significant, especially given the rising incidence of type 2 diabetes and hypertension, which are both consequences of the obesity epidemic.  Additionally, some experts have suggested that an association between these conditions and autism may be explained as the adverse effect of elevated blood sugar, or "hyperglycemia."  We know that excess glucose causes a range of disturbances at the molecular level and that some of these could plausibly impact nervous system development in utero. This realization proves nothing, but "biological plausibility" is an important consideration for an candidate theory about autism. 

Finally, we must keep in mind that even if a causal relationship between metabolic conditions and autism is found, the majority of mothers of affected children are not hypertensive, diabetic or obese, suggesting that important as this association may be, it accounts at best for a fraction of children and families afflicted with this challenging developmental problem.


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