By: William Parker, PhD
A fascinating study was just published by the University of Fukui. It made some news headlines, which tout claims like "Scientists May Have Discovered the Cause of Autism."
Unfortunately, these headlines were entirely misleading and had nothing to do with the actual study or seemingly with the scientists’ intentions who performed the study.
But the bait-and-switch headlines were successful. They got me to read the study.
Understanding the Study from University of Fukui
So what did the scientists actually find?
The authors found yet one more factor associated with inflammation that is also associated with autism. The study team correlated the severity of autism with this factor, a form of the fatty acid called arachidonic acid, present in the blood of babies at the time of birth. Looking at severity rather than just the presence or absence of autism is different than the usual approach, but that’s not what caught my attention.
What caught my attention is that arachidonic acid is the factor connecting the two symptoms of illness treated by acetaminophen: fever and pain. And we already know that acetaminophen exposure in susceptible babies and children causes many if not most cases of autism.
For the technically inclined:
The human body chemically bonds acetaminophen directly to arachidonic acid, creating a new molecule called AM404 that is responsible for blocking pain. And, acetaminophen reduces fevers by blocking the production of prostaglandin E2, a molecule which contains arachidonic acid.
For everyone else:
Acetaminophen is unusual because it treats BOTH fever and pain. One study even called it “unexplained.” We still don't know entirely how it treats fevers, however, arachidonic acid is the common denominator, and is connected somehow to acetaminophen being able to provide both fever and pain relief.
So while arachidonic acid is not the cause, as the news headlines claim, this study might help us understand how acetaminophen induces injury in susceptible babies and children.
The association of the presence of arachidonic acid and severity of autism is very weak, similar to other inflammation-related factors, so for now, we can add it to the ever-expanding list of inflammation-related factors associated with autism.
But it is worth noting.
What Should We Do
Does this tell us more conclusively that acetaminophen exposure in susceptible babies and children (babies and children with inflammation and oxidative stress) causes autism? No, we already know that.
Is it telling us a lot about what’s going on when autism is induced? Maybe. Possibly. But we haven’t understood the message. At least not yet.
For now, the most important thing we can do is to learn about the connection between acetaminophen and autism in susceptible babies and children, tell others about that connection, and make a plan for babies and children under our care.
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