http://www.theatlantic.com/doc/200910u/autism-diagnoses

I’ve seen a few studies that have implied that around 30% of patients with ADHD have comorbid ASD. While searching for those studies, I also came across a study looking at whether there were similar genetic causes between the two disorders, using twins:

http://www3.interscience.wiley.com/journal/119392253/abstract?CRETRY=1&SRETRY=0

I mention this partly because obviously finding genetic correlation between ASD and ADHD, which is already known to have a high genetic correlation, is one more blow against the anti-vax idiots, but more for what they mention about comorbidity, finding that 22% of the children with ADHD also met the criteria for ASD.

How does this relate to that 1% number? Well, multiple reviews have put the worldwide prevalence of ADHD as being around 5% of the population. If 20-30% of those have comorbid ASD, then that 1% statistic starts to make a whole hell of a lot more sense.

I’ve mentioned this before on Dr. Gorski’s other blog a while back, I think, and postulated at the time that 1/166 would be below what one would expect based on comorbidity data with other conditions whose prevalence was better known.

My guess is that eventually (and this will not be anywhere in the near future), some better understanding of the development of dopamine pathways will make all of this make much more sense. Right now all anyone can do is make diagnoses based on symptom presentation. Functional neuroimaging may eventually show that just as people with ADHD have impaired mesocortical dopamine transmission in specific regions of the frontal lobes, there might be far more pervasive issues in people with ASD, maybe looking at mesolimbic dopaminergic activity as well, throughout many areas of the brain.

So where small, localized problems of dopamine transmission might be implicated in ADHD, Tourette’s, OCD, and a few other neurodevelopmental conditions, it wouldn’t surprise me if ASD simply involved more widespread problems in dopamine transmission everywhere.

Of course, armchair speculation about pathophysiology is less important than my original point, which is that this 1% prevalence number is actually somewhat unsurprising if you were to take the data and extrapolate backwards from comorbidities with other conditions whose prevalence is better known. Obviously directly measuring the prevalence of ASD is better than trying to extrapolate from the prevalence of other conditions, but it’s certainly good when the numbers seem to match up between the two.

The problem with most of those studies is that they fail to control for urbanicity, while relying on administrative autism counts. It’s well known that autism is most often diagnosed in urban areas. But it’s probably not the case that autism is actually more common in urban or wealthy areas. For example, a recent prevalence study in a semi-urban area of Sri Lanka found the prevalence of ASD to be over 1%.

Palmer was told about this confound after his first study. In his second study, he did control for urbanicity, and the effect size dropped considerably. Unfortunately, he did not control for urbanicity very well. He treated it as a discrete variable, when in reality, it’s a continuous variable. I’ve suggested these types of studies need to control for (log of) population density.

A final common pathway in essentially all conditions of “stress” is low nitric oxide. Stress in utero does program the brains of experimental animals in ways that would be suggestive of autism-like programming were they to happen in humans. Prenatal stress is strongly associated with autism. Postnatal social deprivation does decrease the number of NO producing neurons in the brains of experimental animals. Exposure to xenobiotic chemicals decreases NO levels. Even exposure to sugar reduces NO levels.

Fever does raise NO levels. I have several blog posts about fever, autism, mitochondrial dysfunction and immune system activation. Nitric oxide physiology is a common pathway that links them all together. Low NO exacerbates autism-like symptoms, high NO ameliorates autism-like symptoms. That is not due to “dysregulation” per se, it is due to good regulation around a bad setpoint. The setpoint is bad because the basal NO level is too low and all NO regulated pathways require the right amount of basal NO to function properly. The NO level can be raised acutely. This has the effect of reducing the severity of the stress responses mediated by low NO (which is a great many of them). This allows neurodevelopment to continue on a higher NO trajectory, on a lower stress trajectory which results in a more neurotypical outcome.

PS Daedalus,
this paper on fever in autism may interest you in case you haven’t already read it: Autism, fever, epigenetics and the locus coeruleus. (http://www.ncbi.nlm.nih.gov/pubmed/19059284)

Your comment misses the point almost entirely.
The post is about the mortal criminal negligence that is being actively encouraged and supported by anti-vax liars, and the delusional followers of their religion.

Discussion of rates of autism are being forwarded to reveal one of their outrageous lies about vaccines.

I had the opposite desire from these statistics, that we shouldn’t be alarmed but comforted that rates are likely not rising. This supports that there might not be some toxin or other agent claiming more and more children each year .

The ‘autism rates rising’ creates alarm and crazy behavior and also has obscured the fact that most children with autism benefit tremendously from behavioral therapies (not from wacko diets, non-vaccinations and chelation). These same claims obscure our understanding of what autism really is.

We should not be alarmed. We should be informed and we should help these children get safe, efficacious treatments in lieu of identifying all the causes of autistic behavior. And finally, we should have done these studies ages ago to actually assess rates of autism across ages.