What Evidence Shows About Tylenol and Autism
Concerns about acetaminophen use during pregnancy largely stem from observational studies, which cannot prove cause and effect.
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Acetaminophen, commonly known as Tylenol, is one of the most widely used over-the-counter medications for pain and fever. It is also considered safe and effective during pregnancy, when untreated pain or fever poses risks to both maternal and fetal health. Obstetricians routinely recommend acetaminophen as an alternative to ibuprofen or aspirin, which can interfere with fetal development and increase bleeding.
Treating pain and fever during pregnancy is medically necessary. For pregnant mothers, unmanaged fever and pain can lead to complications, such as preeclampsia, a potentially life-threatening condition. Untreated fevers can also disrupt fetal development and cause neural tube defects, making acetaminophen the first-line treatment to protect the mother and fetus.
Despite this clinical consensus, President Trump and the U.S. Department of Health and Human Services announced that pregnant women should avoid Tylenol in efforts to tackle the “autism epidemic.” The announcement suggests that prenatal acetaminophen use endangers both the mother and baby. However, a growing body of research indicates autism has no single cause and arises from complex genetic and environmental interactions.
Suggesting that acetaminophen causes autism fuels misinformation and undermines trust in evidence-based clinical guidance.
Concerns about acetaminophen largely stem from observational studies, which identify patterns but cannot prove cause and effect. A recent systematic review evaluated the current literature on prenatal acetaminophen exposure and neurodevelopmental outcomes, including autism spectrum disorder and attention-deficit/hyperactivity disorder. After a PubMed search from February 2nd to 25th, 2025, the researchers identified eight studies specifically assessing autism risk.
The researchers evaluated the risk of bias and the strength of evidence in each study, as shown in the figure below. Risk of bias was rated on factors that could influence an association, including participant selection, study blinding, and exposure assessment. Strength of evidence was rated on a scale from -2 (very weak/no evidence) to +2 (very strong evidence) based on study methods, results, and limitations.
Five autism studies reported a positive link between acetaminophen exposure and autism in children. Two found no association, while one showed mixed results. While the studies had moderately strong evidence overall (+1.17), each exhibited notable weaknesses. One study did not recruit participants consistently across comparison groups, which risked skewing the true result. Several studies also relied on mothers’ self-reports to classify prenatal acetaminophen exposure, which is a method prone to inaccurate recall.
Other studies inadequately controlled for confounding factors, such as maternal age, medication history, or child birth weight, that might also influence acetaminophen use or neurodevelopment. The authors of the review emphasize how methodological limitations can influence the true strength of an association. Although higher quality studies showed positive associations, the authors state they do not warrant broad limitation against prenatal acetaminophen use.
While continued research is needed to understand the biological pathways of acetaminophen, the current evidence does not support causation.
Ann Bauer, a co-author of the review, publicly expressed distress over how it was cited in the HHS announcement. She was “sick to [her] stomach” at the suggestion that pregnant people should avoid Tylenol altogether, and warned that this messaging will cause real harm. Acetaminophen remains the only pain reliever widely considered safe throughout pregnancy, and discouraging its use could leave patients without timely treatment for serious conditions. Bauer also cautioned that overstating preliminary findings risks further eroding trust in science, particularly in autism research, where many mechanisms are still unknown.
Another recent review systematically evaluated over 40 studies on prenatal acetaminophen use, focusing on sibling studies to control for shared genetics and environments. The researchers found no clinical evidence to conclude that prenatal acetaminophen exposure increased the risk of autism in children or other neurodevelopmental disorders. While continued research is needed to understand the biological pathways of acetaminophen, the current evidence does not support causation.
The American College of Obstetricians and Gynecologists echoed this sentiment, emphasizing how untreated pain and fever are much riskier than using acetaminophen as directed during pregnancy. Suggesting that acetaminophen causes autism fuels misinformation and undermines trust in evidence-based clinical guidance. Pregnant people and their families deserve medical care rooted in evidence, not rhetoric that risks doing more harm than good.
This is the second part of a three-part series on autism spectrum disorder. Read the first part here.
