Acetaminophen (known outside the United States as paracetamol) is the medication doctors recommend first for pain and fever during pregnancy. Recent headlines and public claims questioned whether taking it while pregnant raises a child's risk of autism spectrum disorder (ASD) or attention-deficit/hyperactivity disorder (ADHD). A study published in JAMA Internal Medicine on June 29, 2026, tested that question directly and found no such link.

Researchers at the University of Hong Kong analyzed electronic health records for births across Hong Kong from 2001 through 2023. They started with 708,020 mother-child pairs. About 43% of those pregnancies involved acetaminophen use. From that large group, they built two study cohorts: 124,333 children for the autism analysis and 97,285 for the ADHD analysis.

Earlier studies that reported a connection shared a weakness. They compared unrelated families, which leaves room for hidden factors to distort the result. Autism and ADHD both run strongly in families. Autism is roughly 80% heritable and ADHD roughly 74%. Genetics, home environment, and health habits differ from one family to the next, and those differences are hard to measure and account for.

To remove that problem, the team used a sibling-matched design. They compared brothers and sisters from the same mother, where one pregnancy involved acetaminophen and another did not. Siblings share genes and a family environment, so this approach strips out the familial factors that muddy other studies.

In the sibling comparison, acetaminophen use during pregnancy showed no association with either condition.

A hazard ratio of 1.00 means no increase in risk. The results held steady no matter when in pregnancy the medication was used, how much was taken, or how often. Sporadic, intermittent, and persistent use all produced the same flat result. There was no dose-response pattern, meaning higher use did not track with higher risk.

The researchers ran a second check that reframes the whole debate. When they used the standard method that compares unrelated families, they saw the same positive signal reported in past research: a 17% higher autism figure and a 23% higher ADHD figure.

Then they tested acetaminophen use in the year before pregnancy, when the drug reaches no fetus and therefore does not affect fetal brain development. That window still produced a positive signal, 12% for autism and 24% for ADHD.

The authors describe their findings as reassurance about acetaminophen used as directed during pregnancy. Their results line up with sibling-matched studies from Norway, Sweden, and Japan, which reached the same conclusion. Regulatory bodies, including the UK Medicines and Healthcare Products Regulatory Agency and the World Health Organization, have reaffirmed the drug's safety profile in pregnancy.

The alternatives carry real, documented risks. Nonsteroidal anti-inflammatory drugs and opioids are tied to birth defects, low amniotic fluid, neonatal withdrawal, and kidney damage. Avoiding acetaminophen out of unfounded fear leaves untreated pain and fever, both of which threaten a pregnancy, or pushes patients toward riskier options.

The authors advise clinicians to reassure patients that acetaminophen is safe when clinically indicated, used at the lowest effective dose for the shortest time needed.

The data cover prescriptions filled through Hong Kong's public health system. Over-the-counter purchases and private prescriptions went unrecorded. Missing some real use tends to push results toward "no effect," so it works against finding a link rather than manufacturing one. The authors ran additional bias analyses and concluded that this gap does not explain the null result.

A sibling-matched study of more than 100,000 children found no evidence that acetaminophen use in pregnancy raises the risk of autism or ADHD. The positive signals in older research trace back to familial factors those studies could not fully control.