WPLab, Inc.

The struggle to make people aware that acetaminophen is not safe for babies and children is sometimes exciting.

On April 9, 2024, a very misguided paper was published in a VERY prestigious journal (JAMA). Misguided papers are occasionally published despite the best efforts of everyone, so that’s not surprising. In this case, however, the National Institutes of Health (NIH) touted the paper in one of their rare press releases. The NIH funds about 100000 publications per year, but produces less than 20 press releases per year (estimation based on the number of press releases they’ve produced between January and mid-April of 2024), so this was a significant decision.

The JAMA paper claims that acetaminophen does NOT cause autism during pregnancy. The New York Times and other major newspapers carried the headline of the study in when a senior author (the corresponding author) received funding from corporate lawyers working for the leading pharmaceutical company that has manufactured acetaminophen for decades.

But we know that acetaminophen causes many cases of autism at the time of birth, and it probably causes at least a few cases during pregnancy based on other studies. This new paper could be pivotal, changing our thinking. But it is not. The conclusions are not justified by the results.

In the JAMA paper, the authors made two assumptions. They assumed that acetaminophen and the MIA (maternal immune activation, a.k.a. oxidative stress) act independently of each other, that it had to be one or the other. We know based on other scientific studies that this is an invalid assumption. They also assumed that it doesn’t matter if they underestimated acetaminophen use. We know from another study in Sweden (and from other studies in high-income countries) that they probably did dramatically underestimate acetaminophen use.

In science speak: the authors did not apparently appreciate the pharmacology of acetaminophen, which caused them to treat cofactors as confounding factors, and caused them to disregard the importance of under-reporting acetaminophen use in their analysis.
What’s exciting about this (yes, exciting!) is that this gives us yet another opportunity to demonstrate that exposure of susceptible babies and children to acetaminophen really is causing autism. We have just completed the formal proof demonstrating the error.

The answer is….

IF 50% of all cases of autism are induced by acetaminophen use during pregnancy in susceptible women, and IF 90% of susceptibility factors are considered in the analysis and acetaminophen use correlates with those parameters, and IF 60% of women used acetaminophen, but only 7.5% reported using it,
THEN, the analysis shows that acetaminophen does NOT cause autism. (Science speak: HR = 0.992, p = 0.886)

Keep in mind that this is a computer simulation with PERFECT data. In other words, we know absolutely that 50% of autism is induced by acetaminophen in this artificial data set, but under conditions which are possible and even likely in the recent study published in JAMA, even with 50% of all autism induced by acetaminophen during pregnancy, the calculations used in the JAMA article show that acetaminophen is safe for use during pregnancy.

It will take us weeks to incorporate the results into a manuscript for peer review. We will try to publish the paper in JAMA, and will publish it elsewhere if JAMA declines to publish our proof of error. That could take months or even a year or longer.

Our previous conclusions, now published in several pediatric journals, still stand. Exposure of susceptible babies and children to acetaminophen still causes many if not most cases of autism.

And, to answer the big question for now: acetaminophen use during pregnancy at high levels may still be risky, but it’s not nearly as risky as giving acetaminophen to babies and small children. We set the computational analysis at 50% of all autism induced by acetaminophen during pregnancy to prove a point. There is no way that this much autism is induced during pregnancy. Most of it happens after pregnancy.

You can review the evidence for yourself by going to preventautism.org

The problem with autism research: How do we know what to believe?

We just published a new paper in the journal “Children” that can be found here: https://www.mdpi.com/2227-9067/11/1/44. This paper says that acetaminophen causes many if not most cases of autism, and that it’s entirely reasonable that it causes the vast majority of cases. This paper even identifies the period of greatest sensitivity to acetaminophen, the first 10 days of life. It goes on to point out that humans are susceptible starting sometime during pregnancy and ending about age 4 or 5. The paper is doing well, with over 900 views on ResearchGate in less than 3 weeks.

We strongly encourage everyone to look at this paper. It is written so that the average parent-to-be or grandparent-to-be can understand the main points. We used one of the figures from the paper to make the image shown with this post.

Then, just a few days ago, a paper by Megan Woodbury (University of IL at Urbana-Champaign) came out that said that acetaminophen use “may be related to problems with attention in early childhood.”: https://pubmed.ncbi.nlm.nih.gov/38199313

The conclusions in these two papers sound much different. One says that acetaminophen definitely causes many cases of autism, and it’s reasonable that it causes the vast majority. The other says that acetaminophen “may be related to problems with attention”. Can both be correct? The answer is, absolutely yes. Professor Woodbury only looked at exposure to acetaminophen during pregnancy. If you’ve glanced at our paper in Children, you already know that acetaminophen exposure during pregnancy is not as dangerous as exposure at other times. UNLESS, of course, the exposure happened minutes to a few hours before birth, in which case the newborn infant alone must process any drug not processed by the new mother.

I think we have an answer about what to believe when it comes to research on autism. The problem has been the classical problem with microbiologists studying an elephant. Many people are doing great work, but nobody is looking at the big picture. To understand all of the studies, a look at the big picture is necessary. Our most recent paper in Children paints the big picture. https://www.mdpi.com/2227-9067/11/1/44

AUTISM NEWS: Expert testimony for prosecutors was thrown out of court by Judge Denise Cote, effectively halting the largest lawsuit against Tylenol’s manufacturer claiming that their drug caused autism when used during pregnancy. Was that the right decision?

I am not a legal expert, so, like most scientists, I don’t know exactly why judges choose to reject or accept expert testimony. But I am a scientist who has been working on the effects of acetaminophen (the active ingredient in Tylenol) for a decade. I can judge the science, and I can tell you that no peer-reviewed publication or publications tell us clearly that acetaminophen exposure during pregnancy causes autism.

Our best guess, published in the peer-reviewed literature, is that, during pregnancy, acetaminophen use possibly causes up to 10% of all cases of autism, but almost certainly not more than 20% of cases. We just can’t be certain. The data are simply not strong enough for anyone to draw a firm conclusion.

So, from a scientific perspective, the judge made the right decision.
But, at the same time, we know that acetaminophen causes many if not most cases of autism. We have published that in the peer reviewed literature, and will continue to publish more.

“Many if not most” is a bit fuzzy. That could be 20%, 50%, or 80%. What’s the actual number?

One thing tells us that acetaminophen causes virtually all cases, the vast majority of cases, of autism. This one thing is called Occam’s Razor. William of Occam, who, like many great scientists in the “Dark Ages”, ran into trouble with organized religion for his efforts, explained that science is the quest for the simplest explanation that fits all of the observations. This way of thinking has been critical in the history of science, as pointed out recently by Professor Johnjoe McFadden in the Annals of the New York Academy of Sciences (Ann N Y Acad Sci. 2023, 1530:8-17.). Using Occam’s Razor, we can conclude that autism spectrum disorder is, essentially, synonymous with acetaminophen-induced neurodevelopmental injury. That’s a view that we explained in 2017 (J Int Med Res. 2017, 45:407-438).

More recent papers, both published and soon to be published, support that view.

But what about the trial? Why do I agree with the judge if I have concluded that the best fit of all available data is that almost all autism is caused by acetaminophen? The problem is in one detail… a HUGE detail.

The key to the problem is that the judge considered information that applied ONLY during pregnancy. The data regarding Tylenol causing autism at some point in development is overwhelming. There is no question. It’s a scientific fact. And the data tell us that minutes to days AFTER birth is the most critical, and that acetaminophen can also induce autism during the first four to five years of life. On the other hand, data showing that autism can be induced during pregnancy are, by far, the weakest.

Imagine a criminal trial in which overwhelming evidence told us that Joe Banana (a hypothetical criminal) robbed a house while a family was away on vacation. But, in this trial, the judge could only consider evidence that he robbed the house at lunchtime. The best evidence showed that he probably robbed the house late at night or in the early morning hours, but that evidence could not be presented because the prosecution was strictly focused on the robbery happening at lunchtime.

The reason for this bizarre situation is rooted in our legal system and how science trickles into that legal system, mediated in large part by media coverage of published scientific articles. In this case, the prosecution’s hands were tied. They were legally bound to direct the focus of their case on pregnancy. And the judge made the correct decision from a scientific perspective. Bravo, Judge Denise Cote.

For now, Joe Banana will go free. But the evidence is there. Nobody and nothing can cause autism in more than 2% of the population and get away without leaving evidence. Indeed, the overwhelming evidence is already in plain sight, published in the scientific literature. We already have a couple of scientific papers in the peer reviewed literature summarizing that evidence, and we have another one coming soon. It’s just a matter of time before the legal system catches up.

We have LOTS of updates on our work to tell the world that acetaminophen exposure in susceptible babies and children causes many if not most cases of autism.

First, we have a paper coming out in the flagship South Korean pediatric journal “Clinical and Experimental Pediatrics” which outlines 20 lines of evidence allowing us to conclude that many if not most cases of autism are induced by acetaminophen. The paper has been accepted for publication and is already posted on their website. This is our fifth peer-reviewed paper on this topic. We are building the case!

Second, we have started Instagram and YouTube accounts to describe and educate about all of the evidence that acetaminophen exposure in susceptible babies and children causes many if not most cases of autism. You can follow us on Instagram at and on YouTube at .

Third, experiments at the University of North Carolina (UNC) are underway! Already we have shown that acetaminophen is about 10-times more toxic in very young laboratory rats than in adult laboratory rats. You can get a sneak-peak of this data on the long video in our YouTube channel (). It is shocking to know that the toxicity of acetaminophen in very young laboratory animals was NEVER EVALUATED until we did it at UNC. This is really shocking since it’s the world’s most popular drug for babies.

More news is to come, as we have more exciting things waiting in the wings over the next few months. We're going to try and update you here more frequently, so check in regularly for news and information. We're so glad you're here!

Babies and children are far more susceptible to acetaminophen-induced brain injury than a fetus inside a mother-to-be. But yet, the on-line conversation (and discussion of our scientific work) is dominated by concerns about use of acetaminophen during pregnancy. When considering the connection between acetaminophen and autism, the world has literally become confused about the difference between a baby and a pregnant woman. The situation is surreal.

Our first Facebook post on the connection between acetaminophen and autism was in July of 2016. At that time, the problem with acetaminophen was almost unknown. Now the discussion has gained public attention, but it’s off track, with all of the focus on exposure during pregnancy. And acetaminophen continues to cause injury to susceptible babies and children. For more information, see our website at WPLaboratory.org.

We have concluded that acetaminophen (the active ingredient in Tylenol) use in babies and children causes many if not most cases of autism. Does this have anything to do with the lawsuits about Tylenol during pregnancy? Strangely enough, mostly NO. The key is when the autism is induced. Based on all available data, we draw the conclusion that most cases of acetaminophen-induced autism happen AFTER birth, not during pregnancy! It’s a rough guess, but maybe 5 to 10 times more cases of autism are induced after birth than during pregnancy.
So, don’t be distracted by the debate surrounding the lawsuits concerning Tylenol use during pregnancy. Most of the induction of autism happens AFTER birth. For more information, check out our website at WPLaboratory.org.
A new reporter wrote a story about our latest research... and sadly, the biggest comment was from somebody who thought we were talking about use during pregnancy. That is important, but not as important as after pregnancy.

Great strides were made in 2022 connecting autism with acetaminophen (also known as paracetamol, the active ingredient in Tylenol.) Two key papers were published and are cited below.

The key points are:
1. The risk is much higher for babies than for the fetus.
2. We conclude "with no reasonable doubt" that acetaminophen exposure between birth and early childhood causes many if not most cases of autism.
3. A rough guess is that for every 1000 babies and children that feel better taking acetaminophen, about 10 to 15 suffer severe, permanent brain damage.
4. Although most pediatricians believe that the drug is safe when used as directed, it was never proven to be safe in either humans or in laboratory animals. In fact, it is absolutely proven not to be safe in animals, and the evidence that it is not safe in humans is overwhelming.

https://pubmed.ncbi.nlm.nih.gov/35822581/
https://pubmed.ncbi.nlm.nih.gov/35175416/

Paracetamol (acetaminophen) use in infants and children was never shown to be safe for neurodevelopment: a systematic review with citation tracking - PubMed Although widely believed by pediatricians and parents to be safe for use in infants and children when used as directed, increasing evidence indicates that early life exposure to paracetamol (acetaminophen) may cause long-term neurodevelopmental problems. Furthermore, recent studies in animal models....

In our last post, we predicted that helminths would protect people from COVID. We also suggested that, unless somebody tested that idea directly, debate would continue. We were proven correct on all counts... Debate did continue until an almost 3/4 reduction in severe COVID was observed for people in Ethiopia with intestinal worms compared to Ethiopians without worms. Importantly, the worms were not causing any harm as far as the study team could tell.

Our understanding of science allowed us to make predictions in this case! It's important to note that all other scientists making public predictions about what would occur in low-income countries missed the mark, expecting much more damage from viral infections than actually occurred in those countries.

We left that last Facebook post up for over a year, since May of 2020, without posting anything on top of it. That was an important prediction, and we wanted to make sure that anyone interested could easily find it.

We wrote about reconstituting the biome of the human body more than a decade ago. Imagine the decreases in allergy, autoimmunity, and problems with depression and anxiety if everyone had harmless helminths modulating their immune function. And, if the Ethiopian study is any indication, we would have avoided most of the death from COVID. We are working on another paper now, and, based on what we can tell, helminths in the US would have worked even BETTER than they did in Ethiopia to alleviate the COVID pandemic.

This is my last post about helminths on this Facebook site. We are moving on to work on clinical trials with helminths, and those trials do not lend themselves well to social media discussions. Instead, we will be switching this Facebook site to focus strictly on our non-profit work. At the present time, that work centers on the connection between neurodevelopmental disorders such as autism and ADHD and early life exposure to acetaminophen (paracetamol).

Duke Spring break started on March 6th of this year, and our students haven’t yet returned to the lab. So my lab’s work on helminths is closed down for now. We are able to maintain our helminth colony, but nothing more.

At the same time our lab is closed, two rumors are abounding:

1. Many of the fatalities from COVID-19 are due to an overzealous reaction from the immune system. (This is akin to setting off a very large bomb to get rid of a home intruder. Damage to self is highly likely.)

2. People in developing countries are more resistant to this overzealous reaction than are people in Western countries.

It’s a very complicated situation and we just don’t know right now. Maybe it has to do with the relative amount of travel, the age of the population, underreporting, lack of testing, differences in social distancing policies, or other issues.

Not knowing stinks. So, let’s make a prediction and test it. That’s science, which is known to work if employed without too much bias.

We predict that people regularly exposed to helminths will be less likely to die from COVID-19 induced inflammatory cascades than people not exposed to helminths. In fact, people who live with helminths may not die at all from COVID-19 induced inflammatory cascades. It’s a reasonable hypothesis. People regularly exposed to helminths have far less allergy, autoimmunity, and probably neuropsychiatric disease. An over-zealous, self-destructive immune response to SARS-CoV-2 may fall into the same category of disease. Let’s test this one. It’s not as simple as looking at the death toll in India and comparing it to the death toll in the US, but it can be easily done.

We must collect data to test the hypothesis rather than collect data and then hope the answer falls out.

Let’s hope that the hypothesis is correct. We are poised to introduce benign (harmless) helminths into the population. Everything is ready. Such an approach would almost certainly help tens of millions of people with conditions unrelated to COVID-19. Just maybe it would also prevent many serious adverse reactions to SARS-CoV-2.

We don’t know the answer right now. But it would be tragic if we still don’t know in a year from now. It would be beyond tragic. It would represent a major failure on the part of leadership to scientifically explore ways to prevent death induced by SARS-CoV-2.

We have very big news. As a result of one particularly large, anonymous donation*, we now have funding to test the idea that acetaminophen exposure in sick babies can cause permanent neurological damage. To run the experiment, we will be treating rat pups (baby rats) the same as we treat baby humans. The mothers will be fed a horribly good tasting but unhealthy “Western” diet (full of fat and sugar), and the babies will be given an infection with antibiotics. Then the babies will get acetaminophen that is appropriate for their size. Baby rats are about 400 times smaller than a human baby, so 400-fold less acetaminophen will be used for the rats. Yes, we will be up through the night giving baby rats acetaminophen, just the same as parents do with their children.

We know that HEALTHY baby rats get permanent neurological damage from acetaminophen, but we hypothesize that the damage is going to be much, much worse if we give the drug to SICK baby rats. This is not hard to imagine, and is indeed expected based on what we know about the metabolism of acetaminophen. (Explained in our last post.) It seems crazy, but the effect of acetaminophen on a SICK baby lab animal has never been tested before! And our National Institutes of Health declined to consider even looking at the question. (They would not consider even considering a proposal.)

We don’t think it’s a pharmaceutical conspiracy that this issue hasn't been examined, but rather our nation does seem to have developed a sort of “functional insanity” driven by a bureaucratic infrastructure that is completely incapable of responding to desperate need.

This post is made with much gratitude and thanks to our many donors. And a special thanks to the couple who made the donation that gave us the fuel we need for lift-off on this project. It was a substantial sacrifice for them, with sufficient funds to pay for the necessary salaries and fringe benefits of technical personnel. The kindness and love inherent in such sacrifice are a miracle for us.

*The donation was earmarked for this particular study on acetaminophen. We keep our donations for worm therapy separate from our donations for studies on the autism/acetaminophen connection. We are careful about that. (For example, this past Saturday we attended an Immunity's Forge-sponsored fund-raiser for the worm therapy work, and those funds are kept in a separate bin.)