There Is a Postnatal Link Between Tylenol Use and Autism, Researcher Says

The greatest vulnerability arises after birth, when an infant can no longer rely on the mother’s liver metabolism.

Illustration by The Epoch Times, Shutterstock

Recently, Tylenol use during pregnancy has been tied to autism risks, but one expert points to an additional concern.

William Parker, visiting scholar at the University of North Carolina and CEO of WPLab, who has been conducting research on autism for more than a decade, told The Epoch Times that although acetaminophen does present risks in pregnancy, a large body of evidence indicates that the greater risk occurs when it is given postnatally.

When assessing autism risks from acetaminophen, most of the focus has been on use during pregnancy.

The scientific review cited in the Trump administration’s Sept. 22 press conference was conducted by researchers at Harvard, the Icahn School of Medicine at Mount Sinai, and other universities.

“We found evidence of an association between exposure to acetaminophen during pregnancy and increased incidence of neurodevelopmental disorders in children. This association is strongest when acetaminophen is taken for four weeks or longer,” Dr. Andrea Baccarelli, dean and professor of environmental health at Harvard T.H. Chan School of Public Health, wrote in a statement provided to The Epoch Times.

The research includes studies showing that the presence of acetaminophen in fetal stool and cord blood correlates with later diagnosis of autism spectrum disorder and attention-deficit/hyperactivity disorder.

Brian Lee, a professor at Drexel University, told The Epoch Times that there are several observational studies showing an association, but he cautioned that there are no studies that prove causation yet.

“The best science to date indicates that acetaminophen use during pregnancy does not cause autism,” he said.

Baccarelli noted that there is biological evidence supporting the possibility of a causal relationship between prenatal exposure and neurodevelopmental disorders. He pointed to some animal studies showing that prenatal exposure to acetaminophen harms the developing brain.

Some of the evidence refuting the connection between acetaminophen and autism comes from a 2024 Scandinavian study that found no link between acetaminophen use and autism.

However, this study has been criticized by Baccarelli and his colleagues in their recent review for statistical adjustments that may mask true effects.

Parker said that acetaminophen in a healthy child may not cause autism, but children who are biologically stressed are predisposed to being harmed by acetaminophen.

Just as some smokers are more predisposed to developing cancer because of genetics and lifestyle factors, Parker said that controlling for factors such as maternal health and an infant’s genetic susceptibility masks the true effects of acetaminophen.

Postnatal Use of Acetaminophen

Parker, who has more than a decade of experience in autism research, told The Epoch Times that his research indicates that risks also come from acetaminophen use during and after birth.

Acetaminophen is the only pain and fever-reducing medication available to babies younger than 6 months.

In babies who develop autism, Parker said that acetaminophen acts as a trigger amid a sea of factors predisposing health vulnerabilities.

During pregnancy, acetaminophen is metabolized through both the mother’s liver and the fetus’s. The period after birth, when a baby is independent from the mother’s liver metabolism, is when the baby is most vulnerable, he said.

Parker cited a study from the press conference showing that high levels of acetaminophen in cord blood were linked to 3.6 times the odds of autism compared with lower exposures. Cord blood acetaminophen indicates babies’ direct exposure to the medication, when the newborn must metabolize the drug without maternal support.

Some of the evidence supporting a postnatal link comes from early research by Dr. Stephen Schultz. He is the first to look into this connection, focusing on vaccinations and acetaminophen after his son regressed and developed autism following the MMR vaccine and acetaminophen use.

The study, based on a parent survey, found an association between autism and acetaminophen use after vaccination but no link when acetaminophen was not given.

Circumcision has also been linked with autism. Researchers of the paper noted that paracetamol—another name for acetaminophen—is often given to infants for pain relief.

Autism rates began to increase in the 1980s, coinciding with increased prescriptions of acetaminophen. At the time, research indicated that aspirin given to children for fever and pain may lead to Reye syndrome, so public health recommendations shifted to acetaminophen instead.

However, Parker said the full scope of acetaminophen’s effects in babies and children has never been tested.

It was once assumed that babies and children process drugs the same way as adults. Since acetaminophen toxicity in adults manifests as liver damage, investigators then checked only for liver function in infants. However, a baby’s liver metabolism is still immature until age 3.

In adults, acetaminophen is metabolized in the liver through three pathways: glucuronidation, sulfation, and oxidation. The oxidation pathway can create toxic metabolites such as NAPQI, which cause liver and nervous system damage in overdoses.

In babies, the glucuronidation pathway is very weak and not fully active until later in childhood, leaving the sulfation pathway as the dominant safe route for drug metabolism. However, many children later diagnosed with autism also have a weak sulfation pathway. This forces reliance on the oxidation pathway, increasing the risk of toxic buildup.

“We don’t give it to cats because they’re missing [the glucuronidation pathway]. Why are we giving it to babies?” Parker asked.

The body normally uses glutathione to clear toxic metabolites, but research suggests that children who develop autism often have low glutathione reserves—possibly because of predisposing illness or poor maternal health—meaning that toxins are insufficiently cleared.

What’s Next?

Although acetaminophen creates health risks and burdens on the body’s oxidative stress system, it does have an antidote.

N-acetylcysteine, also known as NAC, is an antioxidant given to treat acetaminophen overdose and prevent liver damage. NAC helps make glutathione, which is needed to clear out toxic metabolites.

However, its effectiveness in preventing acetaminophen-related harms in children has not been tested, so it remains only a theoretical antidote.

For pregnant women, acetaminophen is the only pain and fever reducer available, although it is not fully recommended. High fever also poses health risks to both the mother and fetus, including neural tube defects and preterm births.

Baccarelli said that he and his colleagues recommend a balanced approach based on a precautionary principle.

“Patients who need fever or pain reduction during pregnancy should take the lowest effective dose of acetaminophen, for the shortest possible duration, after consultation with their physician about their individual risk-benefit calculation,” he said.

Zachary Stieber contributed to this report.