PSMD NEWSLETTER
DEBUNKING the “debunking” of Tylenol + Autism
October 5, 2025
The media went crazy…
"Fact-checkers" rushed to debunk it.
But here's what they conveniently leave out:
Acetaminophen (Tylenol) has been used since 1886 and given to pregnant women and infants since the 1960s…
And yet serious studies on its effects on the developing brain didn't begin until 2014.
That is insane to me...
For over 100 years, we gave this drug to pregnant women without testing brain effects.
Over 50 studies before approval - all tested liver safety only!
Meanwhile, autism diagnoses went from incredibly rare in the 1940s… to 1 in 31 children today.
The timeline should make anyone raise their eyebrows:
1982-83: Medical switch from aspirin to acetaminophen for kids…
Mid-1980s: Autism rates start climbing…
1990s: Autism explodes
Look, I'm not saying Tylenol explains every single case…
But the convergence of evidence makes it impossible to ignore.
And the biochemistry alone should make you pause.
Here's where the science gets dark...
Your body processes acetaminophen via two distinct pathways:
Adults? Mostly safe route. Manageable.
Babies? Completely different story…
Newborn livers have virtually ZERO glucuronidation capacity for the first few weeks of life.
(Every veterinarian knows domestic cats can't process acetaminophen because they lack glucuronidation. Yet we didn’t connect the dots)
So when acetaminophen crosses the placenta during pregnancy... or when a newborn gets Tylenol directly... most gets shunted through the toxic pathway.
And not just in the liver...
But in the DEVELOPING BRAIN.
Right where cytochrome enzymes turn it into toxic byproducts during the most critical period of neural development.
Add to that the fact that right at birth is the absolute WORST time for exposure...
Before birth, the mother’s liver does the detox work, protecting the baby.
But after the cord is cut? The mother’s protection is gone; the baby’s liver isn’t ready yet to deal with acetaminophen.
They’re completely vulnerable.
And this is why the connection gets missed...
Half of all autism cases are triggered right around birth...
But you don't SEE symptoms until 18-24 months later.
Parents don't connect a Tylenol dose at delivery to regression at 18 months; the triggering event and diagnosis are separated by YEARS.
Now, the obvious question people ask here is…
“Why some kids and not others?”
Many will say it’s just genetics.
But it’s not that simple…
Think about it like this:
If everyone smoked cigarettes, lung cancer would look purely genetic, too.
Some people would get it, some wouldn't. You'd blame their genes for "susceptibility to lung cancer" and completely miss that smoking WAS the trigger.
That's pretty much what's happening with autism and Tylenol if you ask me.
It's so ubiquitous - 40 million adults take it weekly - that it's become statistically invisible.
What's actually genetic? Four critical vulnerability points:
Stack enough of these vulnerabilities... at the wrong developmental window...
And you get the perfect storm for neurological injury.
Still Skeptical? The data is piling up…
“But Paul, what about the studies "DEBUNKING" it?!”
Those studies are incredibly misleading….
Let’s consider the biggest one, which followed 2.5 million Swedish births.
They compared siblings - one exposed in utero, one not. When they did this, the autism association disappeared. (PMID: 38592388)
Keyword here: SIBLINGS!
That means this design controls for shared genetics, shared environment, shared family factors…
So, all this proves is that among families with NO genetic susceptibility to acetaminophen toxicity, the drug doesn't cause autism.
In other words: it’s “safe” if you’re not already genetically vulnerable.
But what about the kids with vulnerabilities?
By design, this study filters them out.
That’s almost like testing peanuts only on people without peanut allergies… then concluding peanuts are safe for everyone 😒
True, for the majority. Useless for those genuinely at risk.
So my hypothesis is thus:
If people stopped using acetaminophen during pregnancy, labor/delivery, and first 3 years (especially first months)...
We could potentially see autism rates drop dramatically within 18-24 months.
I know that’s a VERY controversial statement…
But when you understand that infants can't safely metabolize this drug...
That we weren’t seriously looking into this until 2014...
That the timing of widespread use PERFECTLY matches autism's explosion...
You can't unsee it.
So, maybe we’re right to force this conversation.
Because if there's even a 50% chance this prevents half of autism cases...
Isn't that worth taking seriously?
Welcome to the Remembering 🏹
Paul
