Acetaminophen in Pregnancy and Autism Risk: What Does the Science Really Say?

In fall 2025, public attention was drawn to renewed warnings about acetaminophen (Tylenol / paracetamol) use during pregnancy and possible links with autism and other neurodevelopmental disorders in children. As birth workers, we often receive anxious questions from clients: “Is taking Tylenol in pregnancy going to raise my child’s risk of autism?” It’s a nuanced question. Below is a digest of the most recent evidence, caveats, and practical guidance.

What sparked the renewed concern?

• In September 2025, the U.S. Food and Drug Administration announced it would initiate a labeling review for acetaminophen, citing “evidence suggesting that the use of acetaminophen by pregnant women may be associated with an increased risk of neurological conditions such as autism and ADHD in children.” U.S. Food and Drug Administration
  

• Around the same time, at a public event, some officials amplified fear by stating that acetaminophen use during pregnancy causes autism. Many scientists quickly pushed back, noting that the evidence is far from definitive. Nature+2Science Media Centre+2
  

• Media coverage, policy statements, and “risk alerts” have fueled more questions among pregnant folks. But as with many exposures in pregnancy, teasing apart association vs causation is tricky.

What do the epidemiologic studies show?

Over the past decade, multiple observational studies across different populations have looked at acetaminophen (often self-reported by the mother) and neurodevelopmental outcomes, including autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD). Some studies report modest positive associations; others find no association. Nature+3BioMed Central+3PMC+3

A particularly influential recent study was published in JAMA (2024) analyzing almost 2.48 million children born in Sweden between 1995 and 2019. Drexel University+5PubMed+5PMC+5

Here are key findings:

• In the conventional “population-based” comparison (children whose mothers took acetaminophen vs those who didn’t), there was a marginally elevated risk of autism (hazard ratio ~1.05) and ADHD (HR ~1.07). PubMed+2JAMA Network+2
  

• But the authors then conducted a sibling control analysis (comparing siblings born to the same parents in which one child was exposed in utero to acetaminophen and the other was not). In that sibling comparison, there was no evidence that acetaminophen use was associated with autism (HR ~0.98; 95% CI 0.93–1.04) or ADHD (HR ~0.98). Drexel University+4PubMed+4JAMA Network+4
  

• In other words: when you control for shared familial, genetic, and environmental confounders (by comparing siblings), the small associations seen in broader population analyses disappear. Drexel University+3PubMed+3JAMA Network+3
  

• The authors concluded that the associations seen in non-sibling models may largely reflect familial confounding (unmeasured factors shared by siblings that predispose to both acetaminophen use and neurodevelopmental risk). Lippincott Journals+3PubMed+3PMC+3
  

This is the “European” sibling analysis that is often cited as evidence that—within the same family—one child exposed vs unexposed did not show different autism risk.

Other European population-based cohorts have likewise shown mixed results. For instance, in a meta-analysis of six European birth/child cohorts (≈ 73,881 pairs), prenatal acetaminophen exposure showed associations with borderline/clinical-level symptoms of autism and ADHD; but that kind of analysis cannot correct for all potential confounding. PubMed

In sum: the strongest, most rigorous recent large study (with sibling controls) did not find a link, though some associations remain in less controlled comparisons.

Why is the sibling design so important?

One of the big challenges in drug-or-outcome epidemiology is confounding: mothers who take acetaminophen during pregnancy often do so because of pain, fever, infection, inflammation, migraine, or other conditions that themselves might relate to neurodevelopment risk. If you simply compare children whose moms took acetaminophen vs didn’t, you can’t fully disentangle the effect of the drug vs the effect of the underlying indication or shared genetic vulnerabilities.

By comparing siblings born in different pregnancies to the same parents, a sibling analysis helps “control” for many genetic, socioeconomic, and environmental factors that are shared in a family. If an association persists even in sibling comparison, it is stronger evidence of a causal relation. In the Swedish JAMA study, that sibling-based association was essentially null for autism and ADHD. National Institutes of Health (NIH)+3PubMed+3PMC+3

This is exactly the scenario you requested: a European (Swedish) sibling analysis showing no difference in autism risk between siblings, one exposed prenatally and one not.

How do experts and professional societies interpret the evidence?

Given the conflicting and imperfect data, most professional bodies adopt a cautious, pragmatic stance:

• The American College of Obstetricians and Gynecologists (ACOG) reaffirmed that acetaminophen plays an important and generally safe role during pregnancy when used at the lowest effective dose for the shortest duration needed. ACOG
  

• Some nutrition, environmental health, and epidemiology reviews caution that although associations exist, a clear causal link has not been demonstrated, and possible publication bias or confounding must be considered. Bloomberg School of Public Health+3BioMed Central+3PMC+3
  

• Many commentators point out that the conditions treated by acetaminophen—especially fever, infection, or systemic inflammation—are themselves suspected contributors to neurodevelopmental risk. This makes separating cause and effect especially difficult. PMC+3Science Media Centre+3PMC+3
  

• Some voices argue for greater caution (using acetaminophen less routinely), especially in low-grade symptoms, until further research is settled. Others warn against overinterpreting weak signals and deterring use when needed (e.g. for fever). Bloomberg School of Public Health+3Science Media Centre+3BioMed Central+3
  

In short: no major professional body currently endorses saying “do not use acetaminophen in pregnancy at all” on the basis of autism concerns—but they do emphasize judicious use.

What should birth workers communicate to clients?

Here are some points you might consider when discussing this with pregnant people:

1. Frame it as uncertainty, not alarmism.
   The evidence is still inconclusive and evolving. A good way to phrase this is: “Some studies have suggested a possible association between acetaminophen use in pregnancy and neurodevelopmental risk—but more rigorous analyses, especially sibling comparisons, have not supported a causal link.”
   

2. Explain the sibling-comparison result clearly.
   The Swedish sibling analysis is a powerful piece of evidence: among siblings born to the same mother, one exposed and one not, there was no increased autism risk in the exposed child. That suggests the drug itself is unlikely to be a strong causal agent.

3. Emphasize contextual risk and benefit.

1. Fever, pain, and inflammation during pregnancy are not benign. High fever especially in the first trimester is a known risk for neural tube defects and other complications, and must be managed.

1. Among analgesics, acetaminophen has a long-established safety track record in pregnancy—and alternatives (NSAIDs, aspirin) carry their own risks (especially in certain trimesters).

1. Encourage clients to use the minimal effective dose for the shortest duration, to treat symptoms rather than prophylactically, and always under guidance of a provider.
   

4. Encourage open communication with providers.
   If a client has frequent migraines, chronic pain, or recurrent fever, it’s reasonable to ask whether additional monitoring or alternative strategies are available.
   

5. Avoid overblaming mothers.
   One risk of sensationalizing this topic is that mothers may feel guilt or blame. Emphasize that autism is multifactorial—genetic and environmental factors intersect, and a single exposure is very unlikely to be determinative. The sibling-study result helps reinforce that.
   

6. Stay updated.
   The FDA label review is ongoing, new studies continue to emerge, and meta-analyses may refine our understanding. As birth workers, staying informed helps you respond to clients’ concerns with nuance.

Conclusion

The question of whether acetaminophen in pregnancy increases autism risk is not settled. While some observational studies have shown modest associations, they are vulnerable to confounding. The large Swedish sibling study—comparing exposed vs unexposed siblings born to the same mother—found no difference in autism risk, offering a stronger argument against a causal link.

For now, the best approach is balanced: use acetaminophen when genuinely needed (e.g. fever, pain), at the lowest effective dose for the shortest time reasonable, and always in consultation with a healthcare provider. As birth workers, our role is to support pregnant folks with informed, compassionate guidance, acknowledging uncertainty without fueling undue fear.