Health Conditions
The Latest on Tylenol and Autism: What We Know, How We Know It and What It All Means
Since President Donald Trump announced the connection between acetaminophen and autism, no less than 17 papers have been published in scientific or medical peer-reviewed journals claiming that no evidence supports Trump’s statements. But are those studies valid? Here’s what we know.
By William Parker, Ph.D.
Since President Donald Trump announced the connection between acetaminophen and autism, no less than 17 papers have been published in scientific or medical peer-reviewed journals claiming that no evidence supports Trump’s statements.
The latest of those papers was published in The Lancet on Jan. 16.
ABC News and MedPage Today were among the news outlets that reported on the Lancet study.
The Lancet study and the other papers use the same arguments, drawn for the most part from a study published in JAMA in 2024.
To make sense of everything, it’s easier to explain what we know, then explain the conclusions in those 17 articles.
First, this is what we know.
We know that the combination of acetaminophen (paracetamol), commonly known in the U.S. by its brand name Tylenol, and oxidative stress can and often does induce autism. The equation is simple:
We know that many cases of autism occur when susceptible babies and children are exposed to acetaminophen.
As you can see from the above equation, susceptibility to autism is caused by oxidative stress. Oxidative stress, in turn, can be caused by a multitude of factors, including genetics and environmental exposures, such as infections, toxic chemicals, autoimmune problems and poor nutrition. Even poverty causes oxidative stress.
We strongly suspect that the period of greatest risk is right after birth. Risk extends until the age of about 6 years, when regression into autism becomes very rare.
We also suspect that some risk is present during pregnancy — but it is almost certainly less than the risk immediately after birth.
How do we know all of that?
My laboratory has compiled about 30 lines of evidence allowing us to draw those conclusions.
To be clear, most of those 30 lines of evidence are not from my laboratory. We are solely responsible for some of the evidence. However, the large majority of it comes from other scientists’ laboratories.
To be even clearer, enough evidence existed before 2009 — before I ever even started working on this topic — to know that acetaminophen was probably causing autism. We are much more certain in 2026 than anyone could have been in 2009.
I’ll give you a very, very brief synopsis of the evidence here, lumping several lines of evidence together. If you want a lot more detail, with many more references, please refer to some of our review papers.
1. Pharmacological/toxicological.
- Acetaminophen was considered to be safe only because it was never tested for neurodevelopment. Assumptions of safety were based on liver function. However, studies in laboratory animals show that acetaminophen toxicity is dangerous for brain development, not liver function, in newborns.
- Children with autism produce more of the toxic metabolite of acetaminophen. They literally convert acetaminophen into a toxic metabolite. For review, see Zhao et al.
- Studies have found that children with autism are deficient in a metabolic pathway necessary to safely detoxify acetaminophen in babies (sulfation).
- Genetic, epigenetic and environmental factors associated with an increased risk of autism have an adverse effect on the body’s ability to safely metabolize acetaminophen.
- Acetaminophen is toxic in domestic cats because they lack a particular enzymatic pathway (glucuronidation) that helps safely process acetaminophen. Human newborns are deficient in the same pathway.
2. Clinical observations/epidemiologic work.
- The original study in 2008, which asked whether acetaminophen was associated with autism, found a statistically significant, 20-fold greater risk of regressive autism with acetaminophen use. The confidence intervals in the study were large. But pharmacological/toxicological evidence (see first section above) supporting a causal relationship was already available.
- The levels of acetaminophen in cord blood are very strongly associated with autism. Birth is expected to be the worst time to be exposed to acetaminophen (paracetamol), also known as N-acetyl-para-aminophenol (APAP), based on pharmacokinetic considerations.
3. Laboratory animal studies.
- Studies in laboratory animals from multiple laboratories indicate that early life exposure to acetaminophen is a developmental neurotoxin.
- Early life exposure to acetaminophen has a greater long-term impact on male laboratory animals than female laboratory animals. Autism is more common in males than in females.
- Acetaminophen causes apoptosis-mediated death of cortical neurons in laboratory rats and affects development of hearing and vision. Alterations in cortical neurons and sensory problems are associated with autism.
4. Miscellaneous.
- Acetaminophen alters branching of neurons in culture. APAP and a metabolite of APAP also cause death of brain cells in culture.
- The otherwise unexplained prevalence of autism in orthodox Jews, individuals with cystic fibrosis, circumcised individuals, individuals in countries with shortages of medications, and Danish versus Finnish children are all explained by the connection between acetaminophen and autism shown in the equation above.
- The amount of acetaminophen used in the pediatric population correlates in time with the prevalence of autism. Key events such as the switch from aspirin to acetaminophen and the rise in pharmaceutical advertising explain the time course of the pandemic of autism.
- Acetaminophen temporarily blunts social trust and awareness in human adults. Alteration of social skills is a hallmark of autism.
- The observations of parents that vaccination is associated with regressive autism are explained by the connection shown in the equation above. Parents’ observations have historically been extremely valuable.
- Autism and fetal alcohol spectrum disorder are similar in many regards. Reviewed by Jones et al. Both are induced by a drug that the body converts into a toxic substance.
- Common alternative explanations for acetaminophen-mediated induction of autism are not consistent with known observations and/or require elaborate/complex scenarios to be true.
What does this mean for public health?
The most obvious prediction we can make is that halting the use of acetaminophen during labor and delivery and during the first months of life will profoundly decrease the prevalence of autism.
We also predict that avoiding acetaminophen during the first years of life, until age 6, will further decrease the prevalence of autism.
It is more difficult to predict exactly what might happen if we stop using acetaminophen during pregnancy. Our best guess is that the amount of autism induced during pregnancy is less than 20% of the total, and possibly less than 10% of the total.
But we can predict what the data would look like if acetaminophen use during pregnancy plus oxidative stress leads to autism. In other words, we can predict exactly what to expect if and only if the equation above is true during pregnancy. This is what we would get:
This graph shows previously published data from a computer simulation that demonstrates what would happen if acetaminophen plus oxidative stress causes autism.
We can see the risk of autism on the left, where oxidative stress and acetaminophen combine to cause autism. In this case, use of acetaminophen is associated with more autism than use of no acetaminophen.
We can also see what happens if we “adjust for” oxidative stress or factors that relate to oxidative stress, including genetics. As you move to the right of the graph, adjusting for more and more oxidative stress, the risk goes away. This is because acetaminophen, by itself, cannot induce autism. Oxidative stress is required. We published a general (and very long) review of this topic in 2017.
But what about the 17 papers published since Trump made his announcement? They all depend, for the most part, on the Swedish data published in JAMA by the group at Drexel.
Everybody loves that study because it has the most data for analysis, and the most detail in the data. The study is looking at what happens during pregnancy. Here is the actual data for heavy use of acetaminophen during pregnancy, which they found in only about 2% of the population.
As you can see, this is exactly what we would expect to see if our equation is correct during pregnancy.
Again, this is the actual data from the study in JAMA that is being heavily relied upon. The results are very similar to the results from our computer simulation. This is what we predict would happen if acetaminophen is risky during pregnancy.
In other words, the data from Drexel, published in JAMA, are exactly what we expect to see if all of the evidence I provided above, pointing at a causal connection between acetaminophen use and autism, is relevant to pregnancy.
Therefore, we include the data from Drexel in our list of evidence pointing toward the induction of autism in susceptible individuals exposed to acetaminophen. That is logical.
This result by itself doesn’t prove anything, but it does add to the rest of the evidence that allows us to draw our conclusions. And it tells us that we understand the system well enough to make accurate predictions. That’s an important test of scientific validity.
However, why then are scientists and regulatory agencies still saying that autism is not associated with acetaminophen use during pregnancy?
We can think of a lot of potential reasons. Maybe they don’t know that acetaminophen toxicity is amplified in the presence of oxidative stress, or that children with autism can’t process acetaminophen safely, or that acetaminophen is a potent toxin for brain development in laboratory animals, or that acetaminophen blunts social awareness in adults?
Or maybe it’s something different.
Before The Lancet article came out, I was interviewed by a reporter at The Epoch Times, about the upcoming article in The Lancet. I explained that the results were exactly what we would expect to see if acetaminophen plus oxidative stress causes autism.
There is no question that numerous factors cancelled out in the analysis published in JAMA and emphasized in The Lancet are indeed connected to oxidative stress.
As we previously reported, a vast body of scientific literature addresses this subject. Cancelled factors associated with oxidative stress include poverty and other issues associated with socioeconomic status, many medications, including morphine and antibiotics, heavy alcohol use, smoking, an elevated BMI, and genetics.
The number of children a woman has borne apparently affects oxidative stress responses during pregnancy. And some common medical conditions, including depression and infections are directly related to oxidative stress.
In other words, a vast body of literature tells us that scientists publishing in the world’s leading medical journals are cancelling out variables that are important. They are cancelling out oxidative stress.
The Epoch Times reporter, Marina Zhang, then contacted the senior author of the study in The Lancet, Asma Khalil, to ask if she would respond to this observation. After all, Khalil had asserted that there was no connection between acetaminophen use during pregnancy and autism, which is the opposite of what the data actually show.
Here is her response, as reported by The Epoch Times on Jan. 16:
“While some argue that these factors may interact rather than confound, the approach is widely accepted as one of the strongest methods for addressing confounding.”
Here, Khalil uses “interact” to mean that oxidative stress plus acetaminophen causes autism, and “confound” to mean that oxidative stress, or some unknown factors related to oxidative stress in the absence of acetaminophen, cause autism.
There is no evidence that would suggest that the latter is true, but this is what Khalil assumed to be true while interpreting her results. Her statement translates as, even though “some argue” that my approach is not correct, it is accepted, so I used it.
If Khalil would discuss the issue with any toxicologist familiar with acetaminophen, she would quickly learn that oxidative stress does interact with acetaminophen.
Another way to look at this situation, using an analogy, is that I hired a gardener to take care of my garden while I was away on a trip. The gardener saw some plants in my garden, assumed the plants were weeds, and sprayed them with the best available weedkiller from the professional garden store. I returned home to find all of my vegetables dead.
The gardener argues that he used the best method to kill weeds. I don’t disagree. But the fact is that he killed all my vegetables using an accepted method to kill weeds. He should have figured out if the plants were weeds or vegetables before he sprayed them with a weedkiller that is known to kill both.
Khalil and many investigators before her should have figured out if those variables were confounding (weeds) or interacting (vegetables) before she cancelled them out using a technique that cancels out both.
One of the beautiful things about science is that it can be used to predict outcomes. The problem now is that even though we can predict outcomes based on overwhelming evidence, regulatory agencies and most scientists don’t understand.
This is not a problem with science, but a problem with something else.
When it comes to studying autism, investigators in the mainstream seem to be doing what everybody else is doing rather than doing science. And families around the world are suffering as a result.
William Parker, Ph.D., retired from Duke University after more than 27 years of research there. Parker is currently a visiting scholar at the University of North Carolina and CEO of WPLab Inc., a 501(c)3 non-profit that conducts research and education on the causes of chronic inflammatory disease in high-income regions.
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