Does acetaminophen cause autism?

Following the latest statements regarding the relationship between acetaminophen (paracetamol) and the risk of developing autism, I decided to investigate whether there is any scientific evidence to support it.

The process followed was this:

• Searching for meta-analyses on the topic, which represent the highest level of evidence available, I found a single article addressing this matter.

• Next, I searched for studies using the keywords tylenol, acetaminophen, and autism, and here I did find quite a few more articles.

The Meta-analysis and Its Conclusions

This meta-analysis is titled: Prenatal Exposure to Acetaminophen and Risk for Attention Deficit Hyperactivity Disorder and Autistic Spectrum Disorder: A Systematic Review, Meta-Analysis, and Meta-Regression Analysis of Cohort Studies.

The study's conclusions are as follows: "Acetaminophen use during pregnancy is associated with an increased risk for ADHD, ASD, and hyperactivity symptoms. These findings are concerning; however, results should be interpreted with caution given that the available evidence consists of observational studies and is susceptible to several potential sources of bias."

It appears that the authors found a link between acetaminophen intake in pregnant women and the risk of developing autism (ASD) and attention deficit hyperactivity disorder (ADHD).

The Scientific Critique

Upon trying to delve deeper into the article and accessing it within the journal where it was published, I found a Letter to the Editor written by Professor Per Damkier, MD PhD, from the Department of Clinical Biochemistry and Pharmacology.

In his letter, the professor highlighted three key points of criticism:

• Paternity and ADHD Risk: Damkier points to a study by Ystrom and colleagues that reported "comparable weak signals" for the risk of ADHD following both maternal prenatal exposure and paternal preconception acetaminophen exposure. Damkier criticizes Masarwa et al. for not discussing this point, which he considers important for the issue of causality and confounding in epidemiological data.

• Critique of the Meta-analysis Methodology: Damkier challenges the decision to perform a meta-analysis, much less a meta-regression, on the selected studies. He argues that the underlying data are highly heterogeneous and subject to bias and confounding factors, making a meta-analysis inappropriate.

• Statements on Teratogenicity: Damkier criticizes a statement in the Masarwa et al. article that mentions "recent alarming evidence on the teratogenicity of acetaminophen." Damkier considers this an "exceptional and unnecessarily opinioned statement" with "substantial implications" for healthcare professionals and pregnant women. He states he is unaware of such evidence and emphasizes that the statement is neither referenced nor supported by the Masarwa et al. paper itself. He demands that the authors adequately substantiate and reference this claim.

Other Scientific Articles

Other studies exist, such as the one by Viktor H Ahlqvist et al. titled: Acetaminophen Use During Pregnancy and Children’s Risk of Autism, ADHD, and Intellectual Disability (JAMA, 2024).

In this study, which investigated 185,909 children exposed to their mothers' acetaminophen consumption during pregnancy, no evidence of a relationship between these facts was found.

In fact, in another review article: Acetaminophen in Pregnancy and Attention-Deficit and Hyperactivity Disorder and Autism Spectrum Disorder (Obstet Gynecol, 2025) by Per Damkier et al., the authors evaluate 56 articles, of which only 9 meet the necessary scientific quality criteria for review, along with 3 meta-analyses. Summarily, the authors found a series of problems in these articles:

• The Studies Have "Traps": Most studies that have reported a positive relationship have severe design problems. There is a large selection bias, meaning the way people were chosen for the study may have influenced the outcome. Simply put, they are not perfectly clean studies.

• Other Factors Were Not Considered (Familial Confounding): The great weakness is that these studies failed to measure or control for all the factors that families share (such as genetics, lifestyle, or the upbringing environment) that, by themselves, increase the risk of ADHD or ASD.

• The Effect Fades When Comparing Siblings: The acid test in science is comparing siblings. When scientists performed analyses comparing children exposed to acetaminophen with their siblings who were not exposed (or had a different exposure), the supposed relationship between the drug and the risk almost completely disappeared.

And obviously, they ultimately conclude that no scientific evidence exists to affirm the relationship between acetaminophen consumption in pregnant mothers and the development of autism in children.

Conclusion

And so, after reviewing this, we conclude that the only evidence that might exist, beyond individual studies conducted in animals, appears to be a highly biased and questionable-quality publication, which in no way conclusively supports the link between acetaminophen consumption in pregnant women and the risk of autism in children. Furthermore, the other conducted studies strongly refute this theory, meaning we can completely discard this theory.