Tylenol and Paracetamol: A Deep Dive into the Autism Connection

If you're tempted to listen to the debunkers, you need to read this right now. They should all be fired. This evidence will shock you to the core.

Click to play President Trump’s announcement dated Monday 22nd September 2025.

Strong Words! Are they justified?

You saw in the clip how anxious some people are to debunk Trump’s statements with the usual Scientism catchphrases: “Just because there are a lot of cases among

• Vaccinated children

• Children whose mother took Tylenol while pregnant

• Babies given Tylenol after birth

Is not proof of cause. We’re just better at diagnosing autism these days.”

In other words, they want us to believe that autism is inevitable, its cause is unknown (but definitely not Tylenol) and the moon is made of green cheese. Also, they are the experts, the president is not, and he is making silly accusations because he doesn’t understand the Rules of Science. People should just keep doing what they’re doing and not worry their little heads.

I have written elsewhere how often Science is used as a means to bamboozle the unwary.

By making his announcement, Trump is playing a master-stroke. He is telling us that yes, non-scientists are fit to assess the risks for themselves when the lives of their children are at stake. You don’t have to listen to the debunking. You don’t have to listen to the media. You have a great big champion on your side who is not going to stand for any more gaslighting of your concerns.

The Products in Question

Acetaminophen and paracetamol are the chemical compounds that Trump is referring to. They are sold in the United States under the popular brand name Tylenol, and in the United Kingdom under the brand name Calpol (for babies and children) and various brand names for adults---e.g. Panadol. They are also found in combination products, so always check ingredients on labels of over-the-counter (OTC) medicines.

The Official White House Statement

It looks like most of the media haven’t read it for themselves, they just take the word of the “debunkers”. And let’s be honest: many Americans harbour such a deep-seated animosity toward Trump that they feel compelled to dismiss whatever he says, regardless of its merit. Here is the official White House Statement:

“The Trump Administration does not believe popping more pills is always the answer for better health. There is mounting evidence finding a connection between acetaminophen use during pregnancy and autism — and that’s why the Administration is courageously issuing this new health guidance. Additionally, the Trump Administration is approving a new treatment option that has been found to improve some autism symptoms. President Trump pledged to address America’s skyrocketing rates of autism, and his team is deploying Gold Standard Science to deliver on this pledge. We will not be deterred in these efforts as we know millions across America are grateful.”

— Press Secretary Karoline Leavitt

Today, President Donald J. Trump joined Administration officials to announce major progress in understanding the root causes of autism, which has exploded in diagnoses over the past two decades, and unveil bold new initiatives to tackle the autism epidemic.

Predictably, the Fake News immediately went into frenzied hyperventilation with their usual smears, distortions, and lies.

FACT: Evidence suggests acetaminophen use in pregnant women, especially late in pregnancy, may cause long-term neurological effects in their children.

• Large-scale cohort studies — including the Nurses’ Health Study II and the Boston Birth Cohort — report associations between in utero exposure and later diagnoses of autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD).

• Scientists have proposed biological mechanisms linking prenatal acetaminophen exposure to altered brain development and adverse birth outcomes.

• Andrea Baccarelli, M.D., Ph.D., Dean of the Faculty, Harvard T.H. Chan School of Public Health: “Colleagues and I recently conducted a rigorous review, funded by a grant from the National Institutes of Health (NIH), of the potential risks of acetaminophen use during pregnancy… We found evidence of an association between exposure to acetaminophen during pregnancy and increased incidence of neurodevelopmental disorders in children.”

• Harvard University: Using acetaminophen during pregnancy may increase children’s autism and ADHD risk

• Johns Hopkins University: Taking Tylenol during pregnancy associated with elevated risks for autism, ADHD

• Mount Sinai: Mount Sinai Study Supports Evidence That Prenatal Acetaminophen Use May Be Linked to Increased Risk of Autism and ADHD

• In 2021, an international consensus statement highlighted “a call for precautionary action,” recommending that pregnant women “minimize exposure” to acetaminophen “by using the lowest effective dose for the shortest possible time.”

However much pressure groups are attempting to “normalize” autism, brain damage that makes your child unrecognizable is not a risk that any parent wants to take.

Has the Scientific Community Ignored Evidence Linking Acetaminophen to Autism?

Discovered in 1878, acetaminophen was forgotten until the late 1940s, when it was rediscovered as a painkiller. Johnson & Johnson’s McNeil Laboratories launched it as Tylenol in 1955, and by 1976, Tylenol had become the leading OTC pain reliever in the U.S.

Today, more than 600 OTC and prescription pharmaceuticals, for both adults and children, contain acetaminophen, making exposure virtually unavoidable in modern healthcare. And overdosing is not uncommon. Parents may not realize that cold remedies for children often contain acetaminophen.

As long ago as 2008, a study by Schultz and colleagues found that children given acetaminophen after MMR vaccination were significantly more likely to develop autism than those given ibuprofen. The study surveyed parents of 83 children with autism and 80 controls, finding that autistic children were eight times more likely to have become ill after the MMR vaccine and six times more likely to have received acetaminophen for those reactions.

Crucially, the researchers found that children who regressed into autism were four times more likely to have taken acetaminophen after vaccination. This suggested the drug, not the vaccine itself, might be the critical factor in triggering developmental regression.

Flawed Analysis Of The Data

Some researchers are now saying that the reason for marginalizing the data connecting autism with acetaminophen is because it has been mishandled. A new paper on Preprints.org argues that most studies on acetaminophen and child development—about 82% of them—have made the same mistake. Researchers treated factors like poverty, infections during pregnancy, or certain medications as “confounding variables” and adjusted for them in their analyses.

But according to this new paper, these factors don’t confuse the results—they actually interact with acetaminophen to increase risk. By adjusting for them, researchers may have erased the very signal that shows how acetaminophen could cause harm.

Ethical Concerns

The paper’s authors systematically reviewed 64 papers containing the words “autism” and “acetaminophen” in PubMed searches. Only 23 percent of the papers concluded that there was any need to warn patients.

The authors argue that even if absolute proof is lacking, the potential magnitude of harm—given acetaminophen’s widespread use—justifies immediate changes to clinical practice. They note that acetaminophen has no proven long-term benefits, making risk-benefit calculations particularly important.

The authors acknowledge that establishing causation in complex neurodevelopmental disorders is challenging, and requires balancing precautionary approaches and evidence-based decision making. But this does not excuse a systematic failure to properly evaluate acetaminophen’s neurodevelopmental risks.

References

• Schultz et al. (2008): https://doi.org/10.1177/1362361307089518

• Viberg et al. (2013): https://doi.org/10.1093/toxsci/kft329

Additional references can be found in the original preprint at https://www.preprints.org/manuscript/202508.0006/v1

A Perfect Storm

In 2009, researcher Peter Good published a comprehensive review in Alternative Medicine Review building upon Schulz’s controversial 2008 study and presenting a provocative theory about how timing, biology, and public health policy may have inadvertently created a perfect storm to unleash an epidemic of acetaminophen-related neurodevelopmental disorders.

Good’s most compelling evidence was the synchronous rise of acetaminophen use and autism rates beginning around 1980. Until that point, approximately 50-60% of autistic children showed abnormalities from birth, with 40-50% regressing around 18 months. After 1980, total autism frequency increased ten-fold by 1995, with regression-type autism skyrocketing to “considerably more than 10 times its 1980 level.”

This dramatic shift coincided precisely with acetaminophen replacing aspirin for paediatric use. In 1980, CDC studies linked aspirin to Reye’s syndrome, a rare but often fatal condition affecting children after viral infections. The public response was immediate and dramatic—nationwide sales of children’s aspirin plummeted between 1980 and 1985, while acetaminophen sales surged.

Good noted that specific events affecting acetaminophen confidence were followed by corresponding changes in autism rates. The 1977 FDA liver damage warning coincided with fewer autism diagnoses in children born that year. The 1982 and 1986 cyanide-tampering murders that caused acetaminophen sales to crash were followed by reduced autism rates in children born in 1984 and 1987.

The evidence was converging on acetaminophen like a perfect storm.

The Biological Mechanism

Good proposed a detailed biological explanation for acetaminophen’s potential role in autism. Children metabolize acetaminophen differently from adults, relying primarily on sulphation rather than other detoxification pathways. When sulphation becomes impaired, acetaminophen converts to toxic metabolites that deplete crucial antioxidants like glutathione.

Research by Waring and colleagues had already demonstrated that children with autism have severely impaired sulphation capacity. When given acetaminophen, these children showed reduced urine output, fever, and were “generally off-colour,” suggesting the drug affected them more severely than typical children. Studies found that low-functioning autistic children had a lower sulphation capacity for phenols and amines, potentially leading to toxic accumulations of neurotransmitters in the brain.

Pre-Natal Effects

Good also proposed that prenatal acetaminophen use, by impairing sulphation, reduced the conversion of DHEA (dehydroepiandrosterone) to its sulphate form and increased testosterone. This shift could drive autism’s ‘extreme male brain’ pattern: smaller brains at birth (low oestrogen) followed by overgrowth of male-linked structures (high androgens).

The Reye’s Syndrome Controversy

Good’s analysis challenged the aspirin-Reye’s syndrome connection that drove the switch to acetaminophen. He cited work by Orlowski and colleagues showing serious methodological problems in the studies that implicated aspirin, noting that Reye’s syndrome had not been reported until the 1950s despite aspirin’s use since 1900.

Furthermore, Reye’s syndrome not only disappeared from countries like Australia that had stopped giving children aspirin in the 1950s, but also from countries like France and Belgium that continued aspirin use throughout the 1970s-90s. The syndrome’s incidence was already falling by 1979, before the aspirin warnings took effect.

Can Supplements Help?

If acetaminophen depletes sulphation capacity, Good reasoned that increasing the intake of sulphur compounds might help. He suggested magnesium sulphate (Epsom salts) baths, careful oral magnesium sulphate doses, or well-absorbed forms like magnesium taurate. Nearly half of autistic children benefit from vitamin B6 plus magnesium supplementation, which supports the methionine-to-cysteine conversion that is crucial for sulphation.

Good noted that direct cysteine supplementation appears unsafe, as high doses might transport mercury into the brain. Instead, he recommended N-acetylcysteine and glutathione as safer alternatives, along with vitamin C to protect against glutathione depletion.

Good’s findings align remarkably with recent research showing the time around birth as potentially the most vulnerable window for acetaminophen exposure. But he acknowledged that the correlation between acetaminophen use and autism rates, while striking, doesn’t prove causation. France’s continued high autism rates despite aspirin use, suggested the relationship might be complex. However, by 2003, 90% of fever prescriptions for French infants under three months were for acetaminophen, which could potentially explain the persistence of high autism rates there.

One of Good’s proposals was that if acetaminophen fears proved justified while aspirin’s Reye’s syndrome risks were overstated, there may be a case for returning to low-dose aspirin for paediatric fever and pain relief.

Full citation: Good P. Did acetaminophen provoke the autism epidemic? Altern Med Rev. 2009;14(4):364-372.

Available at: https://refp.cohlife.org/_autism/amr.14.4.Acetaminophen_Autism.pdf

William Parker’s Research

Research published in 2024 in the journal Clinical and Experimental Pediatrics https://www.e-cep.org/upload/pdf/cep-2022-01319.pdf reveals a critical blind spot in acetaminophen safety research.

While most studies have focused on prenatal exposure during pregnancy, the greatest danger from this drug occurs after the child is born. The study’s main author, William Parker, estimates that no more than 20% of cases of Autistic Spectrum Disorder (ASD) result from maternal use during pregnancy, and the real number is probably more like 10% or even less.

Parker’s finding redirects attention to infants and young children receiving acetaminophen directly. Newborns in particular are deficient in a metabolic process called “glucuronidation,” involved in acetaminophen metabolism, making them particularly vulnerable to the drug’s toxic effects.

Through animal research, Parker uncovered alarming parallels between laboratory findings and human autism patterns:

• Long-term brain damage and behavioural changes occur following exposure to acetaminophen early in life, at doses similar or equal to those recommended for children.

• Acetaminophen affects the brains of male rats more than female rats; ASD also affects human males more than females.

• Acetaminophen kills brain cells in adult test animals at doses lower than required to cause liver damage.

These findings are particularly concerning because they demonstrate neurotoxicity at therapeutic doses—not just overdose levels—and in patterns that mirror autism’s male predominance.

Parker’s analysis highlighted two key events that lined up with the rise in autism rates:

1. The Aspirin-to-Acetaminophen Switch (1982 onwards): The first was the national campaign to replace aspirin with acetaminophen, which began in 1982 and continued in earnest for several years thereafter. This shift occurred after aspirin was linked to Reye’s syndrome, leading to widespread adoption of acetaminophen as the “safe” alternative for children.

2. Direct-to-Consumer Pharmaceutical Advertising: The second event was a substantial increase in direct-to-consumer pharmaceutical advertising which began in earnest in 1981 but did not gain traction until after 1990. This advertising increased from around $12 million in 1980, when it was still highly regulated, to $47 million in 1990, then $340 million in 1995 and $5 billion in 2006.

Clinical Evidence from Human Studies

Parker’s review synthesized multiple lines of human evidence supporting the acetaminophen-autism connection:

• Circumcision Studies: Circumcision, for which acetaminophen is often taken as a painkiller, is associated with a dramatic increase in the risk for ASD.

• International Overdose Data: An unexpectedly high incidence of ASD was found in South Korea, where pediatric acetaminophen products often contained quantities of the drug that exceed recommended levels.

• Danish Birth Cohort: Analysis of 61,430 babies in the Danish National Birth Cohort uncovered an increased risk of ASD of up to 66% after postnatal exposure to acetaminophen.

• Vaccination Connection: Acetaminophen administered to reduce vaccine side effects was associated with ASD, even when vaccination alone was not.

Unsafe At Any Dose

To illustrate newborns’ metabolic vulnerability Parker draws a striking comparison to veterinary medicine. “Veterinarians know that there is no safe dose of acetaminophen for a cat. Like cats, human newborns lack mature metabolic pathways to safely process acetaminophen. The brain rather than the liver is the main target organ for toxicity in newborns, contrary to the adult pattern where liver damage is the primary concern. Acetaminophen rapidly kills laboratory rat pups without hurting their livers, a fact that nobody knew when they started putting this into babies.”

Why the Signals Were Missed

Parker’s analysis attributes the delayed recognition of these risks to several factors:

• Research Focus Misdirection: Most research to date has focused on acetaminophen use during pregnancy rather than the more dangerous postnatal exposure period.

• Early Warning Ignored: A report that children with severe ASD could not safely process acetaminophen had already been published in 1999, but its significance was missed entirely, even by the study’s authors.

• Institutional Neglect: When a 2008 study identified the connection between ASD and acetaminophen use during vaccination, it was largely ignored, with no follow-up from the National Institutes of Health, the CDC, or the Pediatric Academy.

• Investigative Approach: Parker suggests that if healthcare workers had investigated like detectives instead of relying only on narrow medical methods, they likely would have spotted these links much earlier.

Risk-Enhancing Factors

The research identified several conditions that increase acetaminophen’s toxicity and autism risk:

• Genetic Factors: Individual genetic variations may affect the ability to eliminate acetaminophen before it causes harm.

• Oxidative Stress: Conditions including infections and various drug treatments can exacerbate the drug’s effects.

• Fasting: Fasting enhances acetaminophen toxicity, a potential problem when a baby is too sick to eat.

Implications for Clinical Practice

Parker’s findings suggest that what has long been considered a benign, essential medication for children may actually pose significant neurodevelopmental risks, particularly during the critical early months and years of life when brain development is most active.

The analysis calls for urgent reevaluation of acetaminophen’s risk-benefit profile in paediatric medicine, particularly given the drug’s widespread use and the potentially permanent nature of the neurological damage it may cause in susceptible children.

Children’s Health Defense is the main organization campaigning for this reevaluation. Follow their website for more developments.

https://childrenshealthdefense.org/defender/kids-acetaminophen-tylenol-autism/