Fact-Checking RFK Jr.’s Claims on Tylenol and Autism

During a congressional hearing on April 17, Health and Human Services Secretary Robert F. Kennedy Jr. labeled a recent Danish study on prenatal acetaminophen (Tylenol) and autism as “garbage” and called for its retraction. He accused the study of being industry-generated and “fraudulent,” but does this claim hold water? The answer is no. The study in question, published in JAMA Pediatrics on April 13, analyzed national prescription data for over 1.5 million children and found no link between maternal use of acetaminophen during pregnancy and autism diagnoses. Experts involved in the research have explicitly stated that there is no evidence of fraud or industry involvement, and the study’s limitations do not justify calls for retraction.

RFK Jr.’s criticism was primarily based on the study’s reliance on prescription data. However, Dr. Kira Philipsen Prahm, the lead author and a researcher from the Copenhagen University Hospital, emphasized that such data, while not capturing over-the-counter use entirely, does not automatically invalidate results. The study acknowledged that OTC use was not fully recorded, but if acetaminophen was causally linked to autism, it would be unlikely to be concealed by these data limitations. Similarly, Dr. Brian Lee, an epidemiologist at Drexel University, pointed out that Denmark’s restrictions on OTC sales—implemented in late 2013—make prescription data a reliable indicator of actual use during the relevant years. Therefore, Kennedy’s suggestion that the data is fundamentally flawed is scientifically unfounded.

Further, Kennedy’s claim that only 2% of pregnant women in the study took Tylenol is misleading. He cited this figure to suggest that the study’s exposure levels were minimal, but experts clarify that actual usage rates are significantly higher. For example, older Danish studies show that about 50% of pregnant women report using acetaminophen, a figure likely an overestimate based on self-reports, but it indicates substantial commonality of use. Importantly, the new Danish research found no dose-response relationship—meaning increased acetaminophen use did not correlate with higher autism risk, weakening the argument for causality.

Contextual Evidence and Scientific Consensus

Multiple international studies—spanning Nordic countries, Japan, and Taiwan—also agree that there’s no conclusive evidence linking prenatal acetaminophen to autism.
Studies using sibling comparisons and diverse methodologies consistently show that initial associations disappear when accounting for genetic and familial factors, suggesting that shared hereditary traits might explain observed correlations.
Recent reviews by independent researchers underscore that the current body of evidence does not support causality, and no “clinically important” link has been established.

Moreover, critics like Dr. Per Damkier, a Danish professor specializing in clinical research, have pointed out that Kennedy’s claims demonstrate a lack of expertise in epidemiology. The claim that the study relies solely on prescription data ignores the significant restrictions Denmark enacted on OTC sales, making prescription data a valid proxy for typical use during the study period. And, as Prahm and colleagues noted, the study’s extensive size and multiple analyses support its conclusion: prenatal acetaminophen exposure does not increase autism risk.

While critics argue that limitations exist in any scientific study, retraction is justified only in cases of obvious flaws such as deliberate errors or fraud. None of these criteria are met here. Kennedy’s repeated accusations—without evidence—appear aimed more at political influence than scientific integrity. In an era when scientific honesty underpins democratic decision-making, it is vital that claims about public health are based on rigorous evidence, not political rhetoric. Accurate dissemination of scientific findings remains essential to responsible citizenship and the safeguarding of science-based policy.