By DStvp
If someone says that taking Tylenol during pregnancy causes autism for the child and another person says it is not true, how exactly does the brain work to define what autism even is, and what it isn’t?
Simply, correlation studies are not exceptional science, regarding anything with the human brain. Someone can say, listening to bird chirping is good for mental health, and then some healthy people decide to listen to bird chirp when they actually need some mind relief, but find that it does not work. The problem may not be that the initial correlation was wrong, but that if the mechanisms of the human brain is not understood for the state or relays that make some therapies applicable, then correlations maybe null.
Autism and Acetaminophen
There is a new [September 22, 2025] report in The New York Times, Kennedy Said to Focus on Unproven Link Between Common Painkiller and Autism, stating that, “Federal health officials are expected to link rising rates of autism to the use of acetaminophen, the active ingredient in the common painkiller Tylenol, in a report to be released on Monday.”
“Scientists have studied a potential connection for years, but the research so far has yielded inconclusive results.”
“The agency plans to warn pregnant women against using acetaminophen except in case of fever. Because it would be unethical to perform pharmaceutical research on pregnant women, all of the existing research on the effects of acetaminophen are observational, meaning that researchers analyze data on women’s pregnancies and then look at how their children do over time.”
“As a result, researchers cannot account for all of the ways in which women who take Tylenol during their pregnancies may differ from the women who do not.”
“Acetaminophen is considered one of the few safe options to treat pain or fever during pregnancy. Doctors already routinely warn pregnant women against long-term use.”
“This afternoon’s report also is expected to recommend a drug called leucovorin, a form of the B vitamin folate, which has long been known to influence neural development, as a possible treatment for autism.Tyle
There is a [September 14, 2022] article by Tufts University, How Does Acetaminophen Work? stating that, “The most promising, yet still speculative, explanation is that it works on one of the cyclooxygenase (COX) enzymes. Blocking this enzyme at the cause of the pain is the mechanism by which nonsteroidal anti-inflammatory drugs (NSAIDS) work. But the effect of acetaminophen at the pain site is too weak to be responsible for relief. However, acetaminophen might block the enzyme production in the brain, thus blocking the further transmission of the pain nerve impulses.”
“As with other pain relievers except opioids, such as morphine, it has a “ceiling effect” to its pain-relieving abilities. That is, after a certain dose, higher doses do not provide additional pain relief.”
“Fever occurs when something—infection or other causes—triggers the master body control in the brain, the thermoregulatory center in the hypothalamus, to reset core body temperature above the usual 98.6 degrees. Acetaminophen, as well as NSAIDs and aspirin, are thought to affect this regulatory center to decrease body temperature. Again, the mechanism is speculated to be the blocking of the COX enzyme.”
Conceptual Brain Science
Anything acetaminophen does that affects nerve impulses — even for a good outcome to reduce pain — may have a side effect in another area. How so? Neuroscience has established that all brain functions [for human life and experiences] are directly operated by neurons and their [electrical and chemical] signals. Neuroscience also stated that neurons are often in clusters.
Now, assuming that signals are in sets, in clusters of neurons — that is, their collections, as sets and then transportation, within sets and across sets — there is an interdependence that might mean that inducing or inhibiting a collection or a transportation [attribute] could have effect beyond a target.
Simply, it is postulated that sets of signals, not neurons are directly responsible for the organization of information and transportation in the brain. So, a feeling like pain is a certain configuration of [say] a set of signals, the same with a memory or an emotion. Now, if acetaminophen attenuates the configuration for pain, or its ability to be fully transported, changes to [some of the target set or transport of] signals may be carried on to other non-pain functions, resulting in some anomalies.
This concept explains side-effects in general, including for acetaminophen. Now, for the possibility that this ‘side-effect likelihood’ may go further in pregnancy, resulting in autism for the child is not clear. For example, there are several psychiatric medications that cause serious side effects for users. It is possible to theorize the signals makeup for a function, then use that to explore what happens when one signal is switched up or down, and what may result for other functions, where that one signal contributes.
For pregnancy, it is possible to explore this as well, in theory, to look closely at causation, while aiming at the big picture to explain how the human brain works.
The NIH Brain Initiative failed to do this. The Machine Intelligence from Cortical Networks (MICrONS) project failed to do this. Connectomics science or the connectome research to map the brain also failed to do this.
There could be development from conceptual brain science on causation, using empirically-supported data in neuroscience, that some conclusions with pregnancy, autism and acetaminophen may not be the case, but so far there’s nothing from the neuroscience establishment, hence the situation.
An unnecessary map without a theoretical basis for how the human brain works
There is a recent [September 15, 2025] spotlight by The Scientist, A Map of the Impossible: MICrONS Delivers AI and Neuroscience Advances, stating that, “However, the factors that determine how neurons connect and interact following a stimulus remain elusive. One funding agency, Intelligence Advanced Research Project Activity (IARPA), through the Office of the Director of National Intelligence, sought to study brain circuitry to build better machine learning algorithms that could replicate the processes of neurons. Additionally, a subsequent project, Brain CONNECTS, is underway using data and resources developed in the MICrONS study to scale up the findings of MICrONS to capture the whole mouse brain.”
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There is a recent [June 4, 2025] paper in PNAS,
The analgesic paracetamol metabolite AM404 acts peripherally to directly inhibit sodium channels,
stating that,
“Paracetamol (e.g., Tylenol or Panadol) is one of the most widely used pain relievers, yet its mechanism of action remains unclear. While previous studies have focused on the effect of its active metabolite AM404 on the central nervous system (CNS), our research reveals that sensory neurons in the peripheral nervous system can also generate AM404. We demonstrate that AM404 inhibits pain-specific sodium channels in nociceptive neurons, effectively reducing normal and inflammatory pain.
These findings provide insights into paracetamol’s peripheral mechanisms of action and highlight the potential of AM404 as a pain-selective local anesthetic, offering broader implications for pain management strategies.”