Experts warn against linking paracetamol in pregnancy to autism as debate intensifies

A high-profile review into rising autism rates has reignited a debate over whether paracetamol use during pregnancy could contribute to the condition, but experts say it is far too simplistic to blame a single exposure for a deeply complex neurodevelopmental disorder. President Donald Trump announced the results of a review led by U.S. Health Secretary Robert F. Kennedy Jr. that sought to identify environmental factors behind autism’s surge, and he suggested a link to maternal paracetamol use. The medical and scientific communities, however, frame autism as the product of a wide mix of genetic and environmental influences that interact across development, with genetics playing a dominant role.

Paracetamol, sold as Panadol in many countries and Tylenol in the United States, is a common remedy for pain, fever and headache. It remains recommended by health authorities for pregnant women as the first-line analgesic, but the guidance stresses short use at the lowest effective dose. In both the United Kingdom and the United States, roughly half to two-thirds of pregnant or new mothers report using paracetamol at some stage during pregnancy. That prevalence is part of why any discussion of its potential links to autism raises scrutiny and concern among expectant families.

Since the discussion began, several studies have produced mixed results. A Harvard-led review in August concluded that there is some evidence of a link between paracetamol exposure during pregnancy and autism, but it cautioned that other maternal health factors and environmental conditions could also be involved. It stopped short of asserting causality and urged pregnant people to seek individualized medical advice. Meanwhile, a 2024 Swedish study involving 2.4 million children, conducted by researchers at the Karolinska Institute, found no association between paracetamol use during pregnancy and autism risk, underscoring the scientific ambiguity surrounding the issue.

The complexity of autism extends far beyond any single chemical exposure. Gina Rippon, professor emeritus of cognitive neuroimaging at Aston University, has spent decades studying the autistic brain and emphasizes that autism is not a disease with a single cause. In her view, the field resembles a field of haystacks with needles scattered throughout, given the brain’s vast complexity—86 billion neurons and an estimated 100 trillion structural connections. “If you’ve met one person with autism, you’ve met one person with autism,” Rippon notes, underscoring the idea that autism is a spectrum with wide variation in symptoms and trajectories. She argues that portraying autism as caused by a single factor disrespects the diversity of the condition and can mislead families and policymakers alike.

The remarks by Trump and Kennedy come amid broader political and media attention to environmental contributors to autism. Kennedy’s review has highlighted environmental exposures as potentially modifiable factors, while critics warn against drawing conclusions that could stigmatize mothers or affect treatment decisions during pregnancy. Rippon and other researchers caution that the public discourse must anchor itself in robust evidence rather than fear-based narratives that could lead to unintended health consequences, such as under-treatment of fever or pain in pregnancy.

Beyond paracetamol, several other factors have been investigated for possible links to autism. Advanced parental age, maternal health conditions, and exposure to sodium valproate—an epilepsy drug—have all been noted as potential contributors. Yet none of these factors neatly explains the condition's onset across all cases, and many appear to interact with underlying genetic predispositions. The breadth of evidence supports the view that autism is highly heritable. To date, scientists have identified more than 800 genes associated with autism, reflecting a complex genetic architecture that interacts with early brain development and environmental experiences.

The science of autism has evolved significantly since the 1990s, when concerns about vaccines and autism—most famously a now-discredited claim tying the MMR vaccine to the disorder—shaped public discourse. Experts say that episode demonstrated the danger of oversimplifying autism’s origins or conflating correlation with causation. Researchers stress that, despite occasional signals from environmental studies, there is no consensus that a single exposure unlocks the disorder, and policy should be guided by careful interpretation of the totality of evidence.

Prevalence trends add another layer of complexity. In the early 20th century, autism was considered rare, with roughly 0.5 per 1,000 children identified. By the 1980s, diagnostic criteria broadened and awareness increased, contributing to higher reported rates. Between 1998 and 2018, reported prevalence rose dramatically, a rise described by some researchers as a combination of broader recognition and evolving definitions rather than a sudden surge in incidence. In the United States, current estimates suggest about one in 36 children receive an autism diagnosis, while the United Kingdom reports roughly one in 57. Public-health officials caution that such figures reflect diagnostics and recognition as much as true incidence, and the label “autism epidemic” remains controversial among scientists who stress heterogeneity and the need for nuanced interpretation.

Folate and folic acid exposure around conception and early pregnancy has also been studied for potential protective effects against autism, with mixed results. Some large Norwegian, American and Israeli studies suggest that maternal folic acid supplementation could be associated with a lower autism risk in offspring, implying a possible protective role for brain development. However, other large studies, such as the Danish National Birth Cohort, have not observed a significant association. Rippon notes that these inconsistencies highlight the perils of drawing firm conclusions about prevention from observational studies alone, especially when randomization and the ability to rule out confounding variables are limited.

Another area of debate concerns potential treatments or early interventions that could alter developmental trajectories. Some social media narratives have promoted unproven approaches, including the idea that certain medications could ‘cure’ autism. Medical experts caution against treatments that lack robust evidence and emphasize that the goal of interventions is to support communication, social engagement and functional skills, tailored to individual needs rather than to “cure” a condition that is defined by biology and experience.

Rippon argues that the most valuable progress in autism science comes from advances in genetics, large-scale sequencing and computational power that enable researchers to map the intricate networks underlying brain development. The pace of discovery has accelerated as teams assemble large cohorts and share data, moving the field toward a more precise understanding of how genetic variation interacts with early-life environments. This work reinforces the view that autism is not reducible to a single cause or cure, and that policy and clinical practice should reflect its diversity and complexity.

As the political and scientific discussions continue, advocates for autistic people and their families stress the importance of accurate information and careful interpretation. Removing stigma and avoiding blame is crucial, not only for the well-being of mothers who fear contributing to their child’s condition, but also for encouraging families to pursue appropriate medical care and early intervention services. The promise of genetics research remains substantial: by identifying how specific genetic profiles influence brain development, scientists hope to improve diagnostics, support, and outcomes for people on the autism spectrum.

In the end, experts say, the narrative around autism must acknowledge both the potential environmental contributors and the dominant role of genetics. While investigations into maternal exposures, including paracetamol, contribute to the broader understanding of autism, they do not erase the breadth of evidence that autism arises from a constellation of factors rooted in biology and development. Rippon frames the takeaway plainly: autism is far more than any single exposure or medication, and policy and public health guidance should be grounded in comprehensive, peer-reviewed science rather than simplified headlines.