Broken Trust: The Tylenol Cover-Up That May Have Damaged Millions of Children

How a once-“safe” painkiller became a prime suspect in the autism epidemic – and why evidence was ignored for decades.

Sayer Ji

Read, share, and comment on the X post dedicated to this thread here: https://x.com/sayerjigmi/status/1966659933694296412

This is Part III in our series.

Part I: Breaking: Government Finally Admits Tylenol-Autism Link After Years of Corporate Cover-Up

Part II Tylenol and Autism, Part II: The Swedish Study That Got It Wrong

Part IV: Tylenol: From Painkiller to Empathy Killer

Key Takeaways

• A maverick scientist under fire: Immunologist William Parker, Ph.D. has spent years arguing that acetaminophen (Tylenol) given in infancy and early childhood — not just in utero — is a major trigger for autism in susceptible children (1), a stance long dismissed by mainstream medicine as fringe (2). An Atlantic article recently cast Parker as an outsider with “outrageous” ideas, even as U.S. health officials consider publicly affirming a Tylenol-autism link (3).
• Mounting evidence vs. medical denial: A growing body of peer-reviewed research and epidemiological data supports Parker’s warning. Laboratory animal studies consistently show acetaminophen’s neurotoxicity (especially in males), and population studies have found correlations between acetaminophen exposure and autism. In one 2008 study, children given acetaminophen after the MMR vaccine had a dramatically higher rate of regressive autism than those given ibuprofen (4). Meanwhile, health authorities and medical organizations — heavily influenced by pharmaceutical interests — have long insisted “no clear evidence” links Tylenol to neurodevelopmental harm (5), even as autism diagnoses have exploded from ~1 in 150 children in 2000 to 1 in 31 today (3.2% of U.S. 8-year-olds) (6).
• A flawed study “debunking” the link — debunked: A widely cited 2024 Swedish cohort study in JAMA initially seemed to refute the Tylenol-autism connection, finding that adjusting for dozens of factors (“confounders”) erased the observed autism risk from prenatal acetaminophen use (7). Parker’s team contends this conclusion got it tragically wrong. Their analysis shows those “confounding” factors were actually indicators of susceptibility — conditions like inflammation and oxidative stress that make a fetus or child vulnerable to acetaminophen’s harm (8). In essence, the Swedish data inadvertently demonstrated that acetaminophen only causes autism when combined with certain risk factors — exactly what Parker’s multifactorial model predicts (8).
• Reckoning and rebuttal on both sides: With an official U.S. policy shift looming — Health Secretary Robert F. Kennedy Jr. reportedly plans to acknowledge an acetaminophen-autism link, sending Tylenol maker Kenvue’s stock plummeting (9) — the battle over “the science” has intensified. The Atlantic profiled Parker as RFK Jr.’s “Tylenol-autism whisperer,” suggesting his evidence isn’t rigorous enough and that he operates at the fringes of academia (2). Parker and allies have fired back with detailed rebuttals: pointing out omissions and inaccuracies in the media coverage, highlighting potential conflicts of interest (e.g., a Duke University CEO and President also sat on Tylenol’s board at the time Parker’s lab was shut down (10)), and emphasizing that no medical advice is being given beyond urging regulators to act on the science.

The Making of an “Outsider”: William Parker vs. the Establishment

In reality, Parker’s credentials and research output tell a different story. Far from a lone crank, Parker spent nearly 28 years on Duke’s faculty and authored almost 200 scientific papers over his career (10). Even after his lab’s closure, he remains productive: in 2024 alone, Parker and collaborators from at least five universities published four peer-reviewed studies related to acetaminophen’s risks and other important topics (1, 8, 11, 12). Two of those papers dealing with acetaminophen’s risks (1, 11) have been viewed over 35,000 times each — an unusually high readership for scientific articles, indicating widespread interest. Parker’s recent publications appear in reputable journals and include co-authors from Duke, UNC Chapel Hill, Northern Kentucky University, and others. This context undercuts the narrative of Parker as an isolated fringe actor.

If his work has faced unusual resistance in the publication process, it may say more about the sensitivity of his topic than the quality of his science. Multiple journal editors have indeed fast-tracked rejections of Parker’s manuscripts for dubious reasons (“formatting errors” or “inappropriate subject matter”), and at least one reviewer dismissed his data as “bizarre” while blandly asserting Tylenol’s safety — all before the weight of evidence was even considered (10). Such experiences, which Parker has spoken about publicly, illustrate the academic bias against challenging the medical status quo.

That bias isn’t merely theoretical. Parker’s clash with Duke University’s leadership suggests that commercial interests and institutional politics may have played a role in marginalizing his research. In 2021, Duke abruptly declined to renew Parker’s contract and shut down his laboratory — even rejecting an offer from an anonymous donor to fully fund Parker’s salary and experiments to keep the lab open (10). Internal emails from Duke’s Department of Surgery revealed that keeping Parker’s acetaminophen-autism research was deemed “not in [the] strategic best interest” of the department (10).

Why would a university turn away outside funding for a productive scientist? One clue: at the time Parker’s lab was forced out, two high-level Duke administrators — including the Chancellor for Health Affairs — were simultaneously serving on the Board of Directors of Johnson & Johnson, the then-parent company of Tylenol (10). Both had been on J&J’s board since the early 2010s. This entangling of interests was reported by The Epoch Times and acknowledged by Parker. It raised eyebrows: was Parker’s work threatening to a major corporate donor or stakeholder? Duke has never confirmed any link between the boardroom and Parker’s fate, but the optics are hard to ignore. Parker himself suspects he was “ousted” for pursuing research that challenged a pharma-funded scientific status quo (10).

“Mistakes have been made, but the individuals treating fevers based on what they were told are not the ones who made those mistakes.” — William Parker, reflecting on how parents and doctors were misled to overuse Tylenol (and stressing that blame lies with flawed science and policy, not those who trusted it).

Despite these setbacks, Parker didn’t quit. He founded a nonprofit research outfit (“WPLab”) and continued investigating the acetaminophen-autism connection outside the ivory tower. If anything, being freed from Duke made him more vocal. By mid-2025, as rumors swirled that HHS under RFK Jr. would vindicate his warnings, Parker was simultaneously excited and cautious. He had long sought mainstream recognition of the hazard, yet he understood the stakes: acknowledging Tylenol’s role in autism could spark panic, lawsuits, and finger-pointing.

Parker has repeatedly emphasized that no one should jump to unscientific or punitive responses. Parents who gave their children Tylenol in good faith are not at fault — they followed standard medical advice. Pediatricians who recommended it were likewise acting on prevailing guidance. “We are not blaming the parents or the physicians,” Parker urges; the focus should be on correcting policy and informing future choices, not guilt or shame (13). He also stresses that medical decisions should be made with a doctor: even knowing what we know, there are situations (like severe infections or high fevers in pregnancy) where the benefits of acetaminophen might outweigh risks. The science isn’t yet able to prescribe clear alternatives in every scenario. In Parker’s words, “many uncertainties about the use of acetaminophen exist” and it’s “not [his] job to tell individual patients and doctors what to do” (13). His job, as he sees it, is to ensure that regulators, physicians, and the public are aware of the science — all of the science — so they can make informed decisions going forward (13).

What the Evidence Really Says: 30+ Lines of Indication, One Coherent Story

So what is this evidence that transformed William Parker from a mild-mannered immunologist into a crusader against Tylenol? In public statements and in materials he provided to journalists, Parker has outlined at least 30 lines of evidence tying acetaminophen to autism. These span epidemiology, animal experiments, biochemical studies, and intriguing population patterns. Individually, many of these findings are associations; none “prove” causation on their own. But collectively, Parker argues, they form a powerful consistent picture — “the total weight of evidence is overwhelming,” he says (1, 8, 11). Let’s summarize some of the most compelling pieces:

• The Schultz study (2008): The first major epidemiological signal arose from a parent-led survey published in Autism by Dr. Stephen T. Schultz et al. Schultz was a dentist-turned-PhD whose own child had regressive autism after an MMR vaccination. Suspecting the culprit might not be the vaccine itself but the acetaminophen given to manage post-vaccine fever, Schultz surveyed families and found a striking pattern. Children who received acetaminophen after the MMR shot were far more likely to develop autism than those who received ibuprofen or no analgesic (4). In fact, among children who experienced post-vaccination fever or other reaction, those treated with Tylenol had about 8 times the odds of autism compared to those not given Tylenol (OR ~8.2), and no increased autism risk was seen with ibuprofen (4). The association was strongest for regressive autism (children who seemed to develop typically but then lost skills): by one measure, a 20-fold greater incidence of regressive autism was linked to acetaminophen use in the 12–18 month age window (4).
• Laboratory animal studies — belated, but unanimous: It sounds unbelievable, but for decades no one tested acetaminophen’s effects on the developing brain — not until the 2010s. When scientists finally did, the results were alarming. In 2013, the first such study (14) found that newborn mice given two doses of acetaminophen had permanent cognitive impairments: later in life, those mice could not learn to navigate a simple maze, a task normal mice master in a day or two (14). Since that pioneering experiment, at least 15 more studies in mice and rats — by independent laboratories around the world — have examined acetaminophen’s neurodevelopmental impact. Every single one found evidence of harm. The observed effects include impaired learning, altered social behavior, and increased anxiety in rodents exposed to pediatric-equivalent doses of acetaminophen early in life (13). Crucially, multiple studies discovered that male animals are far more affected than females (1) — mirroring autism’s male predominance (around four boys are diagnosed for every one girl). As Parker dryly points out, if acetaminophen were a new drug today, these animal results alone would likely halt its development. A drug that consistently causes brain damage in infant mice — particularly males — would never be approved for human infants under current FDA standards (15). Yet acetaminophen has been used in babies for over 60 years, simply because no one had checked thoroughly for neurotoxic effects until recently.
• Biochemistry and the “toxic metabolite”: Why would a pain reliever hurt the brain? Parker and other experts note that infants are uniquely vulnerable to acetaminophen’s pharmacology. The drug is primarily metabolized via a pathway (glucuronidation) that is immature in human newborns — the same deficiency that makes cats famously unable to handle Tylenol (1). As a result, babies (like cats) clear acetaminophen less efficiently, shunting more of it into an alternate route that produces NAPQI, a reactive metabolite. NAPQI is a potent oxidative stressor — essentially a free radical bomb — which in adults is mostly confined to the liver (causing well-known liver toxicity in overdoses). But in infants, studies suggest the liver may be somewhat protected while the developing brain is not (1). In other words, the assumption of safety that pediatricians relied on (monitoring liver damage as the chief risk) was misguided (16); an infant’s liver can appear fine even as their brain suffers subtle injury. This ties into Parker’s larger hypothesis: autism’s rise might be driven by exposure to an otherwise-harmless drug that, in a subset of children with certain biochemical susceptibilities, effectively “poisons” the brain during critical developmental windows.
• Temporal correlations — aspirin out, Tylenol in, autism up: Autism was almost unheard of prior to the 1930s. It was rare until the late 20th century — then it skyrocketed. Improved awareness and broadened diagnostic criteria explain some of that increase, but historical analyses suggest they cannot account for the full surge (8). Something environmental changed. Parker points to the timeline of acetaminophen’s rise. Acetaminophen (paracetamol) began displacing older painkillers by mid-century; it was approved for U.S. infants in the 1950s. Autism rates edged upward slowly in the following decades. Then, in the 1980s, pediatric medicine all but abandoned aspirin (due to Reyes syndrome fears) and Tylenol became the default analgesic for children. Acetaminophen use in babies and young kids boomed in the 1980s–90s, fueled further by aggressive direct-to-consumer marketing (11). Autism diagnoses began to explode in exactly that period (11). By the early 1990s, autism prevalence in the U.S. was roughly 1 in 1,000 children; by the early 2000s, around 1 in 150; today, roughly 1 in 36 (and as high as 1 in 31 in recent data) (6). It’s a curve that eerily parallels the era of peak Tylenol usage. Correlation is not causation — but lack of correlation usually rules out causation. Here, the correlations across time and geography support the plausibility that something about our modern environment (possibly acetaminophen) truly increased autism’s incidence. One striking anecdote: in countries or communities with very limited access to medications, autism remains extremely rare, far below rates seen in affluent, medically saturated societies (8). For instance, observers in low-resource regions have documented schools where neurodevelopmental disabilities are present but autism cases are almost nonexistent — a phenomenon Parker attributes to those areas’ lack of acetaminophen use during infancy (8).

• Epidemiology beyond Schultz — further human studies: In recent years, larger and more rigorous studies have reinforced the acetaminophen-autism link. Notably, a 2019 NIH-funded study (17) of the Boston Birth Cohort (published in JAMA Psychiatry 2020) measured acetaminophen in umbilical cord blood at birth — an objective biomarker of fetal exposure. The children with the highest cord acetaminophen levels had about 3.6 times the risk of being diagnosed with autism during childhood compared to those with the lowest levels (17). There was a clear dose-response: the more acetaminophen markers in the cord blood, the higher the likelihood of autism or ADHD, even after adjusting for many potential confounders (17). This kind of data powerfully complements earlier survey-based findings and indicates the effect is not just recall bias or coincidence — it’s biologically measurable. Other pregnancy cohort studies (in Spain, for example) have also reported links between prenatal acetaminophen use and later neurodevelopmental problems in children, including autism and hyperactivity (18). In 2021, 91 scientists from around the world (including experts in pediatrics and endocrinology) published a consensus statement in Nature Reviews Endocrinology urging caution in acetaminophen use during pregnancy, given the accumulating evidence of possible harm (19). The medical establishment’s response was telling: the American College of Obstetricians and Gynecologists (ACOG) swiftly pushed back, assuring doctors and patients that Tylenol has “always [been] identified as one of the only safe pain relievers” in pregnancy and that “no clear evidence…proves a direct relationship” between recommended acetaminophen use and developmental issues (5). Essentially, ACOG’s message was “keep calm and carry on” — acetaminophen is safe until definitive proof of danger exists (5). Critics argue this is backward, especially given that ethical constraints make definitive randomized trials impossible; by the time “definitive” proof emerges (usually via decades of epidemiology and mechanistic work), countless children could be affected. For now, ACOG’s stance remains that women should not be frightened away from Tylenol, though it advises using the drug “only as needed, in moderation” — a caveat that, in practice, may not change much.

All told, the evidence can be summarized this way: Acetaminophen is not a proven cause of autism in all children, but it is a very plausible trigger of autism in children who are biologically vulnerable. Those vulnerabilities (genetic, metabolic, or related to early-life stressors) are fairly common in the population — and unfortunately, they overlap with factors that might prompt more acetaminophen use. For example, kids who are sickly (prone to fevers), or who have inflammatory conditions, or certain gene variants affecting liver enzymes, might both consume more Tylenol and be more prone to its toxic effects. This entanglement complicates observational studies. It also explains why, to the question “Does Tylenol cause autism?”, researchers can come up with seemingly opposite answers depending on study design. Which brings us to the Swedish study…

The Swedish Study Saga: Confounding the Confounders

In April 2024, a massive study by Ahlqvist et al. in JAMA tracked 1.8 million Swedish children to examine connections between prenatal acetaminophen use and neurodevelopmental diagnoses (autism, ADHD, intellectual disability). At first glance, its conclusions seemed to exonerate acetaminophen — and media headlines touted it that way. The study did find that children of mothers who heavily used acetaminophen in pregnancy had about a 20% higher incidence of autism (and ADHD) than children of non-users (7). However, the authors wrote this off as due to confounding factors: when they adjusted for a long list of 30+ variables (maternal health, genetics, socioeconomic factors, etc.), the acetaminophen-autism link disappeared. Their final verdict: any association between Tylenol and autism is likely explained by other factors (perhaps the underlying conditions that led the mothers to take pain relief, or genetic predispositions), not the drug itself (7). This study was quickly cited by skeptics as the nail in the coffin for the Tylenol-autism hypothesis — association is not causation, and here even the association could be explained away. The Atlantic’s Bartlett, for instance, referenced the Swedish findings to suggest Parker’s theory hadn’t met the burden of proof, quoting a biostatistician as saying “bold claims require rigorous, reproducible evidence” — implying Parker didn’t have it (2).

Parker’s camp, however, saw the Swedish data not as a refutation but as a tragic misinterpretation. From their perspective, the JAMA study’s methodology all but guaranteed a false negative result. (8) Why? Because the variables the authors treated as “confounders” — factors like parental psychiatric history, infections during pregnancy, etc. — are in Parker’s view the very risk factors that make a child susceptible to acetaminophen’s effects. In statistical terms, the study over-adjusted for what are actually mediators or moderators of the drug’s impact, not independent confounders. Parker’s team used an in silico modeling approach to demonstrate the issue (8). They created a simulated population in which acetaminophen was, by design, a major cause of autism (accounting for 50% of cases in combination with certain risk cofactors). When they applied a Cox regression similar to the Swedish study — adjusting for those very cofactors (like infections, inflammation markers, etc.) — the model showed “little to no risk” from acetaminophen (8). In other words, if you statistically remove the contribution of all the things that make a child vulnerable to Tylenol-induced autism, you will inevitably conclude Tylenol was harmless. It’s a bit like arguing that matches don’t cause fires, because once you adjust for the presence of dry wood, oxygen, and arsonists, the match’s effect vanishes. Those factors aren’t confounders; they’re part of the causal chain.

Parker elaborates that in the Swedish dataset, many of the adjusted variables (such as maternal illnesses, or the need for pain medication) likely signaled which pregnancies had oxidative stress or other issues — precisely the conditions under which acetaminophen could do damage (8). When the authors concluded “association does not equal causation, there’s no legitimate evidence linking acetaminophen with autism,” Parker felt they had effectively proven his point: if the prenatal environment is ideal (no risk factors), Tylenol use doesn’t result in autism. But how often is the environment ideal? The Swedish women who took acetaminophen were an unusual subset (only ~7.5% reported use, far lower than expected), perhaps self-selected by having pregnancy complications or pain issues. In a baby without any susceptibilities (a perfectly healthy mom, no genetic risks, etc.), Tylenol might indeed have no observable effect on neurodevelopment — something Parker actually agrees with. What matters is that when susceptibilities are present, Tylenol can push those children over the threshold into autism, and those cases are being “adjusted out” in large epidemiological studies. With heavy use of acetaminophen during pregnancy, the Swedish dataset (7) showed an astounding 87 percent increase in the prevalence of autism… before the factors were adjusted out that should not have been adjusted out.

It’s a nuanced argument, but the implications are huge. Parker’s group went so far as to publish that the Swedish study’s conclusion is “sadly and tragically wrong,” cautioning that it gave a false sense of security and delayed action (8). They stress that plenty of “other evidence, both abundant and robust” firmly demonstrates acetaminophen’s role in autism — evidence that should not be dismissed due to blind spots in any single cohort analysis (8). Some observers might ask: could the Swedish authors have been biased or under pressure, given how their paper’s spin conveniently aligns with industry interests? There’s no direct evidence of foul play; what’s clear, though, is that their interpretation was highly conservative. It fits a historical pattern of authorities leaning toward “everything’s fine” conclusions until incontrovertible proof forces a change.

Tylenol and Autism, Part II: The Swedish Study That Got It Wrong

Sayer Ji

Sep 7

Part I: Breaking: Government Finally Admits Tylenol-Autism Link After Years of Corporate Cover-Up

Read full story

Miscellaneous Evidence: Facts from the Published Literature that Reinforce the Big Studies

According to Parker, “There’s no way to induce autism in a significant fraction of the population without leaving a trail of evidence. That evidence is abundant, for those who look.” As examples, fetal alcohol spectrum disorder and autism share many factors in common, including connection with a pain reliever and fever reducer: alcohol and acetaminophen both reduce pain and fever, and both are converted by the body into a toxic metabolite (8). And, it’s the same enzyme in both cases, called “CYP450 2E1”, that creates the toxic metabolite. In addition, most pediatricians are unaware that acetaminophen has a particularly disturbing off-target effect in adults: It dampens social awareness (23). So, for unknown reasons, acetaminophen is known to affect parts of the brain related to social awareness, which are also profoundly affected in autism. Perhaps as concerning is the observation, dating back as far as 1999 and subsequently confirmed, many children with autism have problems with yet a second pathway, sulphation, necessary to detoxify acetaminophen (24). In a nutshell, evidence dating back more than 25 years had already shown that children with autism have sensitivity to acetaminophen.

Turning Point: From Dismissal to “What If We Were Wrong?”

As of late 2025, exactly one century after Grunya Sukhareva first described autism spectrum disorder, we find ourselves in a remarkable moment. What was fringe is edging toward official acknowledgment. Over the summer, news leaked (via Wall Street Journal) that HHS Secretary RFK Jr.’s team was preparing a report linking acetaminophen use in pregnancy to elevated autism rates (3). Kenvue (the company now owning Tylenol after a Johnson & Johnson spinoff) saw its stock price nosedive 9% on the rumor (9). The company’s interim CEO urgently met with RFK Jr. to lobby against the inclusion of Tylenol as an autism risk, insisting “there is no clear link” and citing conventional medical wisdom that the drug is safe (9). HHS responded cautiously that no final determinations had been made and any claims were “speculative” until the report’s release (20). In public, Kenvue continues to deny any causal connection, pointing to researchers who see the evidence as inconclusive (9). Yet the very fact that the federal government is considering such a stance marks a seismic shift. If HHS “follows through and does the right thing,” as one attorney put it, it could even influence ongoing litigation — there are lawsuits by parents alleging Tylenol caused their children’s autism (currently stalled after a judge ruled the evidence insufficient), and an HHS statement might revive those cases.

For families and advocacy groups who believe acetaminophen harmed their children, this moment is vindication long in coming. To others, it’s deeply unsettling: Tylenol is a household staple, used by millions for pain and fever. How do you suddenly warn the public that this trusted medicine might have contributed to a generational epidemic of autism? Some critics fear overreaction — pregnant women avoiding needed fever reducers and endangering pregnancies, or parents shunning all medications and turning to unproven remedies. Parker himself recognizes this concern; he does not want to incite fear-driven decisions. Instead, he calls for targeted, rational responses: for instance, informing parents that alternatives (like ibuprofen for children over 6 months, or non-pharmaceutical comfort measures) could be used first-line for mild fevers or pain, reserving acetaminophen as a true last resort. Hospitals might reconsider automatically giving acetaminophen to mothers during labor and delivery and to newborns (e.g., for circumcision pain, a practice shown to have questionable benefit and which one study associated with a two-fold higher autism risk) (21). And critically, research should urgently focus on ways to mitigate acetaminophen’s toxicity. Interestingly, Parker has floated a potential antidote: the molecule N-acetylcysteine (NAC), a safe antioxidant used in Tylenol overdose treatment, could theoretically be co-administered with acetaminophen to neutralize its toxic metabolite (22). It’s an intriguing idea that, if validated, might allow continued use of the drug without the developmental risks — a compromise solution for a transitional period.

Meanwhile, medical consensus is inching toward change. After years of denying any problem, some experts now admit caution is warranted. The authors of the 2021 consensus statement (whom ACOG once rebuffed) have been joined by more voices calling for updated guidelines. Even the Autism Speaks organization now prominently notes the prenatal acetaminophen link on its website, and mainstream media are beginning to discuss it. A recent CBS News piece, prompted by RFK Jr.’s planned announcement, openly asked “What does the research say about Tylenol and autism?” — a question that until recently was largely taboo in big outlets. The fact that this conversation is happening at all signals the end of blanket assurances of safety.

On the other hand, skeptics within the scientific community warn against prematurely blaming acetaminophen for autism’s rise. They emphasize that autism is multifactorial — a complex interplay of genetics and environment (vaccines, in the author’s opinion, being the primary driver) — and caution that focusing on one factor could oversimplify a very complicated disorder. It’s true: not even Parker claims Tylenol accounts for all autism. Rather, he suggests it could be the major trigger “for nearly all cases” in susceptible kids, effectively the missing piece that, in combination with genetic predisposition and other co-factors, drives the condition (1). Many scientists remain unconvinced that the evidence meets the threshold for such a claim. They argue that if acetaminophen were that impactful, it would be more obvious and easier to confirm (though one might respond that it was obvious in retrospect — we just weren’t looking and didn’t want to see it). This back-and-forth will likely continue as more studies pour in. What’s critical is that future research and policy be guided by an open mind and a precautionary principle. The cost of wrongly exonerating acetaminophen could be measured in damaged brains and lives; the cost of a false alarm about acetaminophen might be discomfort from more fevers or a dip in pharmaceutical sales. The scales of risk aren’t equal.

Conclusion: A Preventable Tragedy — If We Choose to Prevent It

In the end, the Tylenol-autism story is a poignant case of science caught in cross-currents of institutional inertia, corporate power, and genuine uncertainty. It took individual voices — sometimes ridiculed or marginalized voices — to persist in asking the uncomfortable questions. William Parker’s journey from establishment scientist to “outsider” advocate highlights how difficult it is to challenge entrenched medical norms, even with data on your side. But it also demonstrates the importance of perseverance in science. As Parker puts it, “everyone should be aware of the science. ‘The science.'” (13) — a pointed dig at those who invoke “The Science” to dismiss new evidence. Science is not a fixed set of truths; it’s a process of continually testing and revising our understanding. Today’s medical orthodoxy said acetaminophen was the only safe pain reliever for pregnant women and children. Tomorrow’s might recognize that we made a grievous mistake in handing out this drug like candy without adequately considering its effects on the developing brain.

The cautious path forward is becoming clear. Medical authorities should at minimum alert clinicians and parents that acetaminophen may pose neurodevelopmental risks, especially for certain children, and encourage judicious use. Research funders should prioritize studies on who is most susceptible and how to identify them — perhaps one day a genetic or metabolic test could tell which babies must avoid acetaminophen. And in parallel, we need to seek safer alternatives for managing pain and fever in infants and expectant mothers. The goal is to both reduce unnecessary exposure and inform the public of the real risks and safer alternatives, while science catches up. If autism’s surge has taught us anything, it’s humility: we clearly underestimated environmental factors and overestimated the safety of many modern practices. Now we have an opportunity to correct course.

William Parker often notes a final point when discussing this topic: autism itself is not one thing. It’s a spectrum, ranging from subtle social quirks to profound disability. Genetic research shows dozens of genes can predispose to autism, and yet genetics alone have not explained the rise. An environmental trigger like acetaminophen doesn’t contradict the genetic component — it complements it. Under Parker’s model, genetics load the gun, acetaminophen (and perhaps other stressors) pull the trigger. If that model is even partially true, then preventing autism could be as straightforward as changing an over-the-counter drug recommendation. Imagine that: after billions spent searching for autism genes and theorizing about everything from TV to vaccines, the answer might be to simply use less Tylenol for our young and vulnerable. It’s a hypothesis that, if validated, represents not just a scientific breakthrough but a profound preventable tragedy — one that we must have the courage to face.

As the U.S. government and scientific community grapple with the next steps, one hopes they will remember the lesson of past public health U-turns (think of smoking, or lead exposure, or Thalidomide): early warnings often come from the fringe, from voices dismissed as alarmist. And yet, acting on those warnings sooner rather than later could spare countless people from harm. The parents of autistic children — now grown in number — deserve answers. More than that, future parents deserve assurance that we are doing everything possible to reduce avoidable risks to our children’s developing brains. If acetaminophen is truly one of those risks, then recognizing it openly is not about assigning blame; it’s about accountability and progress. The coming reckoning with Tylenol’s legacy may be uncomfortable, but it also carries hope: the possibility that autism’s tide could finally, after decades, begin to turn down. And that would be a historic victory for public health, born from honestly confronting our mistakes.

References

1. Parker, William, et al. “The Dangers of Acetaminophen for Neurodevelopment Outweigh Scant Evidence for Long-Term Benefits.” Children 11, no. 1 (2024): 44. https://doi.org/10.3390/children11010044
2. Bartlett, Tom. “RFK Jr.’s New Tylenol–Autism Whisperer.” The Atlantic, September 9, 2025. https://www.theatlantic.com/health/archive/2025/09/rfk-jr-autism-tylenol-acetaminophen/684136/
3. Wall Street Journal. “RFK Jr., HHS to Link Autism to Tylenol Use in Pregnancy and Folate Deficiencies.” September 2025. https://www.wsj.com/health/healthcare/rfk-jr-hhs-to-link-autism-to-tylenol-use-in-pregnancy-and-folate-deficiencies-e3acbb4c
4. Schultz, Stephen T., et al. “Acetaminophen (Paracetamol) Use, Measles-Mumps-Rubella Vaccination, and Autistic Disorder: The Results of a Parent Survey.” Autism 12, no. 3 (2008): 293–307. https://pubmed.ncbi.nlm.nih.gov/18445737/
5. American College of Obstetricians and Gynecologists. “ACOG Response to Consensus Statement on Paracetamol Use During Pregnancy.” September 29, 2021. https://www.acog.org/news/news-articles/2021/09/response-to-consensus-statement-on-paracetamol-use-during-pregnancy
6. U.S. Department of Health and Human Services. “‘Autism Epidemic Runs Rampant,’ New Data Shows 1 in 31 Children Afflicted.” Press Release, April 15, 2025. https://www.hhs.gov/press-room/autism-epidemic-runs-rampant-new-data-shows-grants.html
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