Although the precise cause or causes of autism spectrum disorder remain uncertain and seem to be a complicated interaction of genetic and environmental elements, President Trump and his anti-vaccine health secretary Robert F. Kennedy Jr.—who both lack any scientific or medical credentials—have chosen to attribute the blame to Tylenol, a widely used pain reliever and fever reducer that has no established connection to autism.
Now, Texas Attorney General Ken Paxton is taking legal action against the producer of Tylenol, Kenvue and Johnson & Johnson, which formerly marketed Tylenol, asserting that they have been “deceptively promoting Tylenol” while being aware that it “contributes to a considerably heightened risk of autism and other disorders.”
To support that assertion, Paxton references the “substantial body of evidence… recently emphasized by the Trump Administration.”
However, there is no “substantial” evidence backing this assertion, only weak correlations and contradictory research. The rationale provided by Trump and Kennedy for blaming Tylenol was disclosed during a disjointed, nonsensical press conference last month, where Trump mentioned a “rumor” about Tylenol and shared his “view” on the subject. Nevertheless, he strongly cautioned against its usage, repeatedly stating: “don’t take Tylenol.”
“Don’t take Tylenol. There’s no risk. Don’t take it. You might be uncomfortable. It may not be as simple, but don’t use it if you’re pregnant. Don’t take Tylenol and don’t administer it to the baby after birth,” he declared.
“Scientifically unfounded”
As previously reported by Ars, some studies have identified a correlation between Tylenol (also known as acetaminophen or paracetamol) usage and an increased risk of autism. However, numerous studies that have identified such a correlation possess significant limitations. Other research found no connection at all, including a highly respected Swedish study that evaluated autism risk among siblings exposed to different levels of acetaminophen during pregnancy while otherwise having similar genetic and environmental risks. Acetaminophen did not show an effect, indicating that other genetic and/or environmental influences may clarify any observed associations. Additionally, even if there exists a true correlation (or correlation) between acetaminophen use and autism risk, that does not imply that the pain reliever is the source of autism.
