Stories describing new relationships occurring within the autism epidemic appear every day. Families wonder about their significance; whether they, in some way, can better understand why their children are affected by the condition (? older fathers, overweight mothers, living near highways, premature births, anxiety, copy number variations, etc.) and the significance of new treatments appearing on the horizon as it applies to their situation.

For example, the report of a “vaccine” FOR autism attracted attention recently.
The good: The thinking goes that killing Clostridia (an especially nasty cootie) with this anti-biofilm product could reduce autistic behaviors in many patients. Importantly, it validates “complementary and alternative” medicine’s insistence on the gut-brain connection in autistic behaviors.
The bad: It’s only been tested in rabbits.
The ugly: “The vaccine might take more than 10 years to work through preclinical and human trials, and it may take even longer before a drug is ready for market…”

Regarding treatment, UC San Diego recently reported “Antipurinergic Therapy Corrects the Autism-Like Features in the Poly(IC) Mouse Model”.
The good: The drug, suramin, targets a cell messaging system that produces a metabolic response to stress. “According to a new theory, autism is strongly linked to this pathway… Scientists in the U.S. found that the drug corrected 17 types of abnormality linked to autism in genetically modified mice, including social behaviour problems.”
The bad: It’s only been tested in mice.
The ugly: Mice aren’t men.

At the SFARI conference this past week in Spain, research was presented that supported the environmental theories of causation.
The good: There were significant presentations reporting associations with air pollutants and insecticides. Also, the topics of proper prenatal and pre-pregnancy vitamin and mineral intake were popular offerings.
The bad: “The new studies showed only associations and couldn’t prove causality, and each factor itself likely accounts for a small portion of the risk for autism, researchers say.”
The ugly: “Genetics likely account for about 35% to 60% of the risk, many researchers say.” Genetics accounting for susceptibility is not that helpful until the downstream abnormality is identified.

The report of placental changes signaling an increased association with later autism got a fair bit of press this week.
The good: The test “…yielded a 92% specificity rate for predicting ASD risk status — and …yielded a 99.9% specificity rate. The differences between the 2 groups were amazingly, awesomely different.” The earlier the red flag, the better.
The bad: “… this test will not be able to identify all individuals who might develop autism.”
The ugly: If we don’t do anything about the red flags that we see already (“Let’s wait until he’s older…”), is this information that helpful?

Another recent article that points to early involvement was Deviance in fetal growth and risk of autism spectrum disorder in the American Journal of Psychiatry.
The good: “… poor fetal growth was more strongly associated with ASD with intellectual disabilities than without. Regardless of fetal growth, preterm birth increased ASD risk.” I repeat, the earlier the red flag, the better.
The bad: In my many years caring for high risk premies and diabetic babies (the very small and very large), when I was Director of our Follow Up Clinic, ASD was not being recognized/diagnosed.
The ugly: Ditto to the last ugly.

The most important points that we can glean from such literature are:

1. More recognition of the epidemic, and therefore more research that will lead to treatments – eventually, even if it’s just avoidance of the toxic offenders.

2. Earlier recognition of red flags that a child may be at-risk, with earlier diagnosis, instead of “he’s a boy – they talk late.” Hopefully that means earlier interventions.

3. More recognition of the medical nature of the condition.


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