Statement from Autism Science Foundation Regarding Wall Street Journal Report  “RFK Jr., HHS to Link Autism to Tylenol Use in Pregnancy and Folate Deficiencies”

(September 5, 2025, 4:00 pm ET) This afternoon, The Wall Street Journal reported that HHS Secretary Robert F. Kennedy, Jr. will announce later this month that Tylenol has been identified as a cause of autism, and that a medicine derived from folate can be used to treat symptoms in some people. Any association between acetaminophen and autism is based on limited, conflicting, and inconsistent science and is premature given the current science. 

Autism doesn’t have a single cause. It is the result of a complex mix of genetics and environment. We know that genetic factors play the biggest role: hundreds of genes have been linked to autism, and inherited or spontaneous changes in these genes can alter brain development. Environmental factors also matter, especially during pregnancy, such as advanced parental age at conception, prematurity or very low birth weight, and exposures that affect brain development, like fever or illness during pregnancy. The best current science shows autism arises from the complex interaction of genetic susceptibility with environmental influences during brain development. 

“It is disingenuous and misleading to boil autism’s causes down to one simple thing. We know that autism is incredibly complicated, and we need to move away from studies that simplify it down to one exposure without any other considerations”, said Dr. Alycia Halladay, Chief Science Officer at the Autism Science Foundation.

The Autism Science Foundation strongly supports research into autism’s causes. More research needs to be done before alarming families or suggesting steps that may not actually reduce risk. Pregnant women deserve clear, evidence-based guidance – not incomplete conclusions that could erode confidence in safe, beneficial care. 

Acetaminophen
In August of this year, researchers at Mount Sinai published a systematic review of 6 studies examining the relationship between prenatal acetaminophen and autism or autism traits in children. Because not all studies were of the same size or included the same analysis, they differed in their results. Based on their analysis, they concluded that there was reason to believe that autism was linked to early acetaminophen exposure, possibly tied to biological mechanisms like oxidative stress, hormonal disruption, and epigenetic modifications.  Other reviews have pointed out some of the methodological concerns of early studies that did not properly control for different variables, including genetics or the “why” of acetaminophen exposure during pregnancy.  Therefore, the researchers cautioned that, while not proving causation, even modest risk increases could have public health implications.

One of the studies included an analysis of 2.4 million Swedish children utilizing a sophisticated design that used siblings as a control rather than a completely different group of children with no family history. This controls for some maternal health factors as well as some genetic influences.  Using a sibling control, any association with autism that was previously seen now disappeared.  This suggests that genetic and maternal health factors are also critical to any documented association with autism. Those findings were also replicated in a week-old study from Japan, which also used a sibling control group to understand the roles of confounding factors like genetics and maternal health on the Tylenol association. Unfortunately, since that study was published just recently, it was not included in the earlier systematic review. If it had been, the conclusions from the Mount Sinai study may have been different.    

Based on existing data, there is not sufficient evidence to support a link between Tylenol and autism. However, as with any medication taken during pregnancy, it should be approached with caution and with the advice of a trusted medical provider.   

Folate
Low maternal folate levels during early pregnancy have been linked in several studies to an increased risk of autism in children, though findings are not entirely consistent. Large prospective cohorts in Norway, the U.S., and Israel found that mothers who took folic acid supplements around conception had children with a 30–70% lower likelihood of autism compared to those who did not, suggesting folate may have a protective effect on brain development,  However, other large studies, such as the Danish National Birth Cohort, did not observe a significant association, and differences in timing, dosage, and measurement of folate exposure may explain conflicting results. Overall, while not definitive, the weight of evidence suggests that inadequate folate during critical windows of pregnancy may increase autism risk, whereas appropriate supplementation likely reduces it.

The suggestion that folate may ameliorate some of the symptoms of autism comes from four randomized controlled trials investigating a drug called leucovorin, which is also known as folinic acid. Unlike regular folic acid, folinic acid can cross into the brain even when folate transport is impaired.  Some studies suggest that folate transport is blocked in some children with autism, resulting in low brain levels of folate, but these findings have been inconsistent. Data suggesting that leucovorin may be effective come from four small randomized controlled trials, all using different doses and different outcomes, and in one case, reliant on a specific genetic variant. This science is still in very early stages, and more studies are necessary before a definitive conclusion can be reached.

ASF Chief Science Officer Dr. Alycia Halladay will discuss these issues on ASF’s weekly podcast to be released Monday, September 8.                                                                  

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Contact Information
CJ Volpe
cvolpe@autismsciencefoundation.org
Autism Science Foundation