Acetaminophen

Is Acetaminophen the cause of Autism?

The first and most fundamental question to ask is this: What is the true value of acetaminophen in health compared with the potential risk if the associated findings are indeed plausible?

Here are some thoughts on autism spectrum disorder (ASD) and acetaminophen/Tylenol for those interested:

The weight of evidence I have reviewed, and remain open to changing with stronger data, suggests that ASD risk is primarily driven by maternal inflammation and immunometabolic factors during pregnancy. Studies show ASD risk increases by 50–400% (depending on the study) in mothers who are obese or diabetic before conception, linking epidemiology to the biochemistry of immune activation. (Ye et al., 2025; Li et al., 2016)

Excessive intake of high fructose corn syrup, sugar, and starch polymers drives metabolic pathways that flood the developing brain with cytokines, affecting microglia and neuronal networks. Think early metabolic syndrome with constant immune activation bathing a newborn’s brain.

Maternal viral illness, such as COVID-19 or influenza during pregnancy, dramatically increases disease risk in certain populations. (Edlow et al., 2023) Obesity and metabolic disease also raise maternal autoantibodies targeting specific brain networks linked to ASD phenotypes. (Ramirez Cellis et al., 2021) Preconception chemical exposures in both parents contribute as well, though likely to a lesser extent. In other words, there are many more biologically plausible causes of ASD than acetaminophen alone. Moreover, ASD is not a single-gene disease like cystic fibrosis or sickle cell anemia; it is a syndrome with likely thousands of unique pathways to its development.

 So, is acetaminophen the cause of ASD?

In my view, the connection is associative, not causative. Women prone to needing antipyretics and analgesics often have underlying immunometabolic conditions that may be the true drivers of disease. That said, acetaminophen is not benign. It depletes glutathione activity, increasing oxidative stress and prolonging the persistence of toxins, thereby fueling a vicious cycle of inflammation. You take the medicine to reduce symptoms, but without addressing root causes, recurrent use follows. Thus, acetaminophen use may be more of a proxy for maternal health status, while its own mechanism, glutathione depletion and potential epigenetic effects, could exacerbate risk in vulnerable settings.

As Dr. William Parker noted:

“The association of ASD with numerous factors that cause oxidative stress, including metabolic abnormalities, genetic polymorphisms, infections, antibiotic use, and other medical conditions, is consistent with the fact that acetaminophen metabolism is more hazardous in the presence of oxidative stress, a condition associated with risk factors for ASD.” (Parker et al., 2023)

His point highlights the fetal vulnerability in states of oxidative stress, increasingly common in industrialized nations. There is clearly smoke here; whether there is truly fire remains to be seen.

Personally, I neither use nor recommend acetaminophen because of its effects on glutathione depletion and potential epigenetic alterations. In a country where ASD now affects roughly 1 in 30 children, we must minimize avoidable risks. Occasional use in pregnancy is likely safe, but repeated or chronic use, particularly in young children, concerns me. Fever is not the enemy; it is a natural defense against infection. Cool compresses can be effective when fevers rise above 103°F. For fevers between 100–102°F, I typically recommend no medication unless otherwise indicated.

One of my colleagues recently asked, What if a pregnant woman has recurrent headaches or pain? Tylenol is all that’s recommended. My response: find and address the root cause first. A single dose is unlikely to cause harm, but repeated use without understanding the underlying issue raises concern. Ultimately, acetaminophen use in pregnancy should be discussed between each patient and her obstetrician, weighing risks and benefits carefully.

Dr. Parker argues that acetaminophen use in pregnancy and early childhood represents a major, not minor, risk for ASD. His recent paper underscores the need for urgent, rigorous study.

"Based on available data that include approximately 20 lines of evidence from studies in laboratory animal models, observations in humans, correlations in time, and pharmacological/toxicological considerations, it has been concluded without reasonable doubt and with no evidence to the contrary that exposure of susceptible babies and children to acetaminophen (paracetamol) induces many, if not most, cases of autism spectrum disorder (ASD). However, the relative number of cases of ASD that might be induced by acetaminophen has not yet been estimated. Here, we examine a variety of evidence, including the acetaminophen-induced reduction of social awareness in adults, the prevalence of ASD through time, and crude estimates of the relative number of ASD cases induced by acetaminophen during various periods of neurodevelopment. We conclude that the very early postpartum period poses the greatest risk for acetaminophen-induced ASD, and that nearly ubiquitous use of acetaminophen during early development could conceivably be responsible for the induction in the vast majority, perhaps 90% or more, of all cases of ASD. Despite over a decade of accumulating evidence that acetaminophen is harmful for neurodevelopment, numerous studies demonstrate that acetaminophen is frequently administered to children in excess of currently approved amounts and under conditions in which it provides no benefit. Further, studies have failed to demonstrate long-term benefits of acetaminophen for the pediatric population, leaving no valid rationale for continued use of the drug in that population given its risks to neurodevelopment." (Parker et. al. 2023)

Dr. Parker will be on the Podcast to discuss this topic next week. Stay Tuned

Ye Lancet Endo Diab

Li Pediatrics

Edlow JAMA

Parker Children

Zhao Clin Exp Ped

Image below from Zhao et. al. 2023