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A lot of heat has been generated lately around whether taking acetaminophen, a.k.a., paracetamol, in pregnancy increases the probability of autism in the child. In this article, I hope to shed some light instead.

Here’s my plan:

I’ll start by laying out the research for and against the connection, so that you can decide for yourself whether there’s a link instead of needing to rely on someone else’s opinion. Be warned: we’ll be looking at a study pooling data from multiple studies that concludes there’s a link between acetaminophen in pregnancy and autism. We’ll also be looking at two studies that conclude that while it may look like there’s a connection, there actually isn’t. This may leave you wondering “Why can’t they make up their minds?” but that’s how research works. You have a theory, you design a study to test whether your theory is upheld by your study’s results, and if it is, then you (all properly done research papers include a discussion of the strengths and limitations of the study) and others, based on the evidence from their own or others’ studies, debate whether your theory was correct, or there are other explanations for your results.

Next, in case you side with the study concluding that acetaminophen in pregnancy does increase autism, I’ll tell you how big that difference is. That will allow you to decide whether the potential benefit in taking it outweighs the harm.

And finally, in the “Takeaway” section, I’ll provide a process to help you reach a decision that’s right for you on whether to take it or not. That’s because it isn’t enough just to have the information. You need to know what to do with it.

If that sounds good to you, keep reading.

What Do the Studies Tell Us?

In recent years, studies and reviews pooling their data have been reporting a possible link between taking acetaminophen in pregnancy and autism in the child. The newest and best of these is a review published just this year that includes eight studies (Prada 2025). Based on the quality of the studies they included and the consistency of their findings, the reviewers concluded there was strong evidence for a relationship between acetaminophen exposure during pregnancy and a childhood diagnosis of autism. The reviewers further buttressed that conclusion with evidence that acetaminophen could plausibly have this effect in that 1) acetaminophen crosses the placenta freely, and 2) animal and acetaminophen metabolism studies support its potential for harmful neurologic effects during fetal development.

Challenging that conclusion are the authors of two studies contending that the seeming connection arises from not accounting for some factors associated with autism in children that are also associated with taking acetaminophen (Ahlqvist 2024; Okubo 2025). As the studies’ authors explain, the underlying reasons for taking acetaminophen such as infection, fever, migraine, and pain from autoimmune disease (e.g. rheumatoid arthritis) are themselves risk factors for neurodevelopmental disorders in children, a problem called “confounding by indication.” Also, it isn’t uncommon to be taking multiple medications in pregnancy, making undetected “confounding by other medications” another possibility. Finally, a predisposition to developing a neurologic disorder is inheritable, and we have evidence that those who have health conditions associated with having a neurodevelopmental disorder are more likely to report taking acetaminophen in pregnancy.

To test the validity of their theory, the two groups of researchers compared autism occurrence rates in full sibling pairs in which one sibling was exposed to acetaminophen during pregnancy, and the other wasn’t. They reasoned that comparing autism rates in exposed versus unexposed siblings would nullify the effect of factors such as parental genetics and maternal health conditions. In both studies, researchers began by comparing outcomes in the total population and finding, as the studies in the review did, that exposure to acetaminophen in pregnancy increased diagnoses of autism. However, when confined to an analysis of sibling pairs, the difference disappeared, which upholds their theory that factors not accounted for may explain the apparent link between acetaminophen exposure in pregnancy and autism in the child.

As a bonus, these two studies also provide data that the studies in the review didn’t: the actual autism occurrence rates in their total populations. This, as I said earlier, is important for weighing potential harms versus benefits when considering whether to take the medication.  In one study, taking acetaminophen during pregnancy resulted in 1 more autism diagnosis per 1,000 pregnancies compared with not taking it (28 vs. 27 per 1,000 pregnancies) (Ahlqvist 2024); in the other, it resulted in 5 more autism diagnoses per 1,000 pregnancies (85 vs. 80 per 1,000 pregnancies) (Okubo 2025). Put another way, if taking acetaminophen in pregnancy increases the risk of autism, then depending on baseline autism diagnosis rates, in the first study, the odds of the child not being diagnosed with autism were 973 out of 1,000 pregnancies with no exposure versus 972 out of 1,000 pregnancies with exposure and 920 versus 915 pregnancies out of 1,000 in the other.

In Summary

A review pooled data among multiple studies. It concluded that acetaminophen exposure increases the probability of autism diagnosis in the child (Prada 2025). The review also reported on data supporting that neurodevelopmental harm from exposure to acetaminophen in utero is biologically plausible.

Two groups of researchers contended that the studies finding a link had not taken into account certain confounding factors associated with both autism and taking acetaminophen (Ahlqvist 2024; Okubo 2025). They theorized that if they were correct, comparing autism rates in sibling pairs, one of whom was exposed to acetaminophen during pregnancy and the other wasn’t, would nullify the hidden effect of those factors. They carried out analyses of autism rates in their respective populations overall and in the subpopulation of exposed/not exposed sibling pairs. The difference they saw in the population overall disappeared when they analyzed sibling pairs, supporting that their theory was correct.

Finally, if there is a difference, it’s small, amounting to 1 excess autism diagnosis per 1,000 pregnancies with fetal exposure to acetaminophen in one study (Ahlqvist 2024) and 5 excess autism diagnoses per 1,000 exposed pregnancies in the other (Okubo 2025).

Your Takeaway

So, now we arrive at how to make sense of this data in a way that helps you make the right decision for you. Under the more typical circumstance of your care provider making a recommendation, applying the BRAIN acronym provides an excellent template for deciding whether you want to agree, decline, or do something else. It goes like this:

Benefits
Risks
Alternatives
Instinct/intuition
No or not now

In this case, though, you are starting with knowing the potential risks, and the dialogue isn’t with your care provider but with yourself. Still, the steps of the process apply; we just need to adapt them a bit.

Risks: You now know there is some question of whether acetaminophen increases the risk of autism. You also know the magnitude of the risk if it does, something you wouldn’t ordinarily know if your care provider was your source of information. That knowledge enables you to make a more nuanced decision. That takes us to the other side of the equation . . .

Benefits: What is the reason you are considering taking acetaminophen, and what are the potential harms of not taking it? For example, as you saw above, fever increases the probability of adverse neurodevelopmental effects, and acetaminophen reduces fever. Your care providers can help you with this piece as well as its follow on . . .

Alternatives: What are the other options for relieving your symptoms, and what are the pros and cons of those? This brings us to the other aspect of decision making . . .

Instinct/intuition: So far, we’ve been talking about taking in and processing information. Sure, the data should inform your decision, but your heart and your gut are as important—maybe even more important—as your thoughts in determining the right decision for you.

No or not now: In this adaptation of your decision-making process, the options are more accurately “no,” “not yet,” or “try an alternative and reconsider the options if the alternative isn’t satisfactory.”

And there you have it. As promised in my introduction, I’ve given you the data and a process to guide you through using it to decide under what circumstances you would take acetaminophen. I’ve also given you something more: I’ve given you a means of determining whose opinions you can trust. You now know how scientific research works, and that gives you a touchstone for evaluating the merits of the advice of others who claim expertise in health care issues. Specifically, you now know that:

1. The point of conducting research is to investigate whether the evidence supports your theory.
2. Part of determining whether the evidence supports your theory is making an open-minded assessment of whether critiques of that evidence are valid.
3. Because every treatment has potential benefits and harms (excepting the rare circumstance when research finds no benefits), recommendations always depend on balancing the potential benefits against potential harms under the specific circumstances for which the treatment is recommended.

Here’s an example of the application of those principles in action: After discussing the strengths and limitations of their analysis, the review’s authors affirm their opinion that the data support a probable link between acetaminophen exposure in pregnancy and autism (Prada 2025). They then conclude their report by saying:

While this association warrants caution, untreated maternal fever and pain pose risk [too], necessitating a balanced approach. We recommend judicious acetaminophen use—lowest effective dose, shortest duration—under medical guidance, tailored to individual risk-benefit assessments, rather than a broad limitation.

In contrast, here’s an example that flouts all three: Doubling down on his judgment that acetaminophen should never be taken in pregnancy, Robert Kennedy Jr dismisses the uncertainties of its relationship with autism, saying (McCreary 2025):

 None of this is dispositive but all of it is stuff that we should be paying attention to. This is not proof. We’re doing the studies to make the proof.

Whose opinion do you think is worthy of trust? The person who understands and abides by those principles or the one whose mind is made up and is looking to “make the proof” to justify what he already believes?

References

Ahlqvist VH, Sjoqvist H, Dalman C, et al. Acetaminophen Use During Pregnancy and Children’s Risk of Autism, ADHD, and Intellectual Disability. JAMA 2024;331(14):1205-14.

Okubo Y, Hayakawa I, Sugitate R, et al. Maternal Acetaminophen Use and Offspring’s Neurodevelopmental Outcome: A Nationwide Birth Cohort Study. Paediatr Perinat Epidemiol 2025.

Prada D, Ritz B, Bauer AZ, et al. Evaluation of the evidence on acetaminophen use and neurodevelopmental disorders using the Navigation Guide methodology. Environ Health 2025;24(1):56.

RFK Jr. Links Circumcision to Autism via Supposed Tylenol Use. MedPage Today, October 10, 2025. (Accessed 10/12/25, at https://www.medpagetoday.com/washington-watch/washington-watch/117885.)