“Acetaminophen doesn’t cause autism. That’s absurd. You have no proof.”

A summary of the scientific evidence showing Tylenol damages the developing brain

If you’ve been with me for awhile, you know I’ve been alerting parents to the harms of acetaminophen, especially when it’s used in pregnancy and infancy, for over a decade.

Though it’s been very hard to get policymakers, doctors, and even parents to pay attention, the scientific evidence that acetaminophen (the main ingredient in baby Tylenol) is implicated in the rise of autism is “incontrovertible,” according to Dr. William Parker, Ph.D.

Fierce backlash

Every time a new study is published providing yet more information about why and how this is not a safe drug for babies, the backlash is fierce.

“I gave my baby Tylenol and he’s fine.”

“Tylenol doesn’t cause autism. That’s ridiculous.”

“My child has severe autism and he never once had Tylenol.”

The first argument is called the “anecdotal fallacy.” My grandfather smoked like a chimney, died at 84, and never got lung cancer. Therefore, cigarette smoking doesn’t cause lung cancer.

The second argument, when we dismiss an idea out of hand by attacking the idea as “crackpot” or “ridiculous,” is called the “invincible ignorance fallacy.”

Just because we stubbornly believe something is true, does not mean it’s true. It does, however, suggest that we humans are stubbornly, willfully, or pigheadedly committed more to our own ignorance (and egos) than to the evidence set before us.

As for the third argument, most people don’t realize that their infants may be exposed to Tylenol by babysitters, family members who don’t agree with their parenting principles, and even by clinicians in the hospital during labor and delivery, circumcision, or the administration of the hepatitis B vaccine or the vitamin K shot. This is likely the time of life when the newborn is most vulnerable to the harms of being exposed to this drug.

Quietly offloading liability

In the meantime, Johnson & Johnson, the company that used to make this toxic drug, quietly sold its consumer health business to a new company called Kenvue in 2022. This split, which was finalized in 2023, effectively protects J&J from the inevitable and profit-crushing liability issues I predict we’re going to be reading about very soon in the mainstream media over the harms of Tylenol.

For both the naysayers and those willing to consider that a ubiquitous over-the-counter medication that “everybody uses so it must be safe” is a causative factor in the autism epidemic, here’s a summary of scientific evidence.

This summary is based on a list compiled by my colleague Dr. William Parker, a widely published immunologist and biochemist who does impeccable scientific research. It is based on one of his recent scientific papers,which is currently being reviewed by his peers.

Print this out and share it with your doctor.

Bring it to your preschooler’s school nurse.

Tell your friends and family.

If COVID craziness taught us anything, we should all know by now that we can’t wait for government regulatory agencies to do the right thing.

To take back your family’s health, it’s time to toss the (baby) Tylenol.

Summary of evidence that Acetaminophen exposure in susceptible babies and children causes autism spectrum disorder

1. Pharmacological/toxicological evidence

(a) Acetaminophen (APAP) was considered to be safe only because it was never tested for neurodevelopment [1]. Assumptions of safety were based on liver function, but studies in laboratory animals (see below) indicate that this is not a valid approach for safety testing in neonates.

(b) Mechanisms of APAP-mediated injury are plausible. Children that are susceptible to injury produce more of the toxic metabolite of APAP. APAP toxicity and ASD are both associated with problems in mitochondrial function, calcium signaling, and arachidonic acid metabolism. For review, see Jones et al. [2, 3].

(c) Numerous studies have found that children with ASD are deficient in a metabolic pathway necessary to safely detoxify APAP in babies (sulfation) [4-6].

(d) Genetic, epigenetic, and environmental factors associated with an increased risk of ASD have an adverse effect on the body’s ability to safely metabolize APAP [6-8].

2. Clinical observations/epidemiologic evidence

(a) The original study in 2008 asking the question whether it was the MMR vaccine or APAP that induced ASD found a statistically significant, 20-fold greater risk of regressive ASD with APAP use [9]. The confidence intervals on the study were large, but pharmacological/toxicological evidence (see Pharmacological/toxicological evidence above) was already available supporting a causal relationship.

(b) The levels of APAP in cord blood are strongly associated with ASD [10]. Birth is expected to be the worst time to be exposed to APAP based on pharmacokinetic considerations [11].

(c) Cohort studies found that use of APAP during pregnancy (numerous studies) and post-partum (one study) has been associated with adverse long-term effects on the mental health of offspring. Almost all studies on this topic have underestimated the impact of APAP due to mistaking cofactors for confounding factors [2]. This mistake has even led some investigators to conclude that acetaminophen is totally safe for brain development. But in doing so, they ignore all of the other evidence.

(d) APAP is not used in domestic cats because they lack a particular enzymatic pathway (glucuronidation) [12-16], making APAP toxic for them. Human neonates lack the same pathway [17, 18].

3. Laboratory animal studies

(a) Numerous studies in laboratory animals from multiple laboratories indicate that early life exposure to APAP is a developmental neurotoxin [19-33].

(b) Early life exposure to APAP has a greater long-term impact on male laboratory animals than female laboratory animals [24, 32, 34, 35]. ASD is more common in males than in females.

(c) APAP causes apoptosis-mediated death of cortical neurons in laboratory rats [36] and affects development of hearing and vision [26, 28]. Alterations in cortical neurons and sensory problems are associated with ASD.

4. Other evidence and mechanisms to consider

(a) APAP alters branching of neurons in culture [37]. APAP [36, 38] and a metabolite of APAP [39] also cause death of brain cells in culture.

(b) The otherwise unexplained prevalence of ASD in orthodox Jews, individuals with cystic fibrosis, circumcised individuals, individuals in countries with shortages of medications, and Danish versus Finnish children are explained by the APAP/ASD connection [2, 11].

(c) The amount of APAP used in the pediatric population correlates in time with the prevalence of ASD. Key events such as the switch from aspirin to APAP and the rise in director-to-consumer advertising explain the time course of the pandemic of ASD.

(d) APAP temporarily blunts social trust [40] and awareness [41] in human adults. Alteration of social skills is a hallmark of ASD.

(e) The observations of parents that vaccination is associated with regressive autism [42, 43] are explained by the APAP/ASD connection. Parent’s observations has historically been extremely valuable [8].

(f) ASD and fetal alcohol spectrum disorder (FASD) are similar in many regards. Reviewed by Jones et al. [2] This proves that a single drug can cause a spectrum disorder similar to ASD.

(g) Common alternative explanations for APAP mediated induction of ASD are not consistent with known observations and/or require elaborate/complex scenarios to be true.

References.

1. Cendejas-Hernandez, J., et al., Paracetamol (Acetaminophen) Use in Infants and Children was Never Shown to be Safe for Neurodevelopment: A Systematic Review with Citation Tracking. . European Journal of Pediatrics, 2022. 181: p. 1835-1857.

2. Jones, J.P., 3rd, et al., Evaluating the Role of Susceptibility Inducing Cofactors and of Acetaminophen in the Etiology of Autism Spectrum Disorder. Life (Basel), 2024. 14(8).

3. Jones, J., et al., Three Mandatory Doses of Acetaminophen During the First Months of Life with the MenB Vaccine: A Protocol for the Induction of Autism Spectrum Disorder in Susceptible Individuals, in Preprints. 2025, Preprints.

4. Geier, D.A., et al., A prospective study of transsulfuration biomarkers in autistic disorders. Neurochem Res, 2009. 34(2): p. 386-93.

5. Pagan, C., et al., Decreased phenol sulfotransferase activities associated with hyperserotonemia in autism spectrum disorders. Translational Psychiatry, 2021. 11(1): p. 23.

6. Alberti, A., et al., Sulphation deficit in "low-functioning" autistic children: a pilot study. Biol Psychiatry, 1999. 46(3): p. 420-4.

7. Frye, R.E., et al., Cerebral folate receptor autoantibodies in autism spectrum disorder. Molecular psychiatry, 2013. 18(3): p. 369-381.

8. Parker, W., et al., The role of oxidative stress, inflammation and acetaminophen exposure from birth to early childhood in the induction of autism. Journal of International Medical Research, 2017. 45(2): p. 407-438.

9. Schultz, S.T., et al., Acetaminophen (paracetamol) use, measles-mumps-rubella vaccination, and autistic disorder. The results of a parent survey. Autism, 2008. 12(3): p. 293-307.

10. Ji, Y., et al., Association of Cord Plasma Biomarkers of In Utero Acetaminophen Exposure With Risk of Attention-Deficit/Hyperactivity Disorder and Autism Spectrum Disorder in Childhood. JAMA Psychiatry, 2020. 77(2): p. 180-189.

11. Parker, W., et al., The Dangers of Acetaminophen for Neurodevelopment Outweigh Scant Evidence for Long-Term Benefits. Children, 2024. 11(1): p. 44.

12. Anvik, J.O., Acetaminophen toxicosis in a cat. Can Vet J, 1984. 25(12): p. 445-7.

13. Savides, M.C., et al., The toxicity and biotransformation of single doses of acetaminophen in dogs and cats. Toxicol Appl Pharmacol, 1984. 74(1): p. 26-34.

14. Court, M.H., Feline drug metabolism and disposition: pharmacokinetic evidence for species differences and molecular mechanisms. Vet Clin North Am Small Anim Pract, 2013. 43(5): p. 1039-54.

15. Lautz, L.S., et al., Metabolism and pharmacokinetics of pharmaceuticals in cats (Felix sylvestris catus) and implications for the risk assessment of feed additives and contaminants. Toxicol Lett, 2021. 338: p. 114-127.

16. St Omer, V.V. and E.D. McKnight, 3rd, Acetylcysteine for treatment of acetaminophen toxicosis in the cat. J Am Vet Med Assoc, 1980. 176(9): p. 911-3.

17. Miller, R.P., R.J. Roberts, and L.J. Fischer, Acetaminophen elimination kinetics in neonates, children, and adults. Clin Pharmacol Ther, 1976. 19(3): p. 284-94.

18. Cook, S.F., et al., Neonatal Maturation of Paracetamol (Acetaminophen) Glucuronidation, Sulfation, and Oxidation Based on a Parent-Metabolite Population Pharmacokinetic Model. Clin Pharmacokinet, 2016. 55(11): p. 1395-1411.

19. Hussin, S. and L. Al-Allaf, Histological changes of CA and DG regions of hippocampus of rats’ brain after exposure to Acetaminophen in postnatal period. Iraqi Journal of Veterinary Sciences, 2022. 36(1): p. 151-158.

20. Harshaw, C. and A.G. Warner, Interleukin-1β-induced inflammation and acetaminophen during infancy: Distinct and interactive effects on social-emotional and repetitive behavior in C57BL/6J mice.Pharmacology Biochemistry and Behavior, 2022. 220: p. 173463.

21. Herrington, J.A., et al., Elevated ghrelin alters the behavioral effects of perinatal acetaminophen exposure in rats. Dev Psychobiol, 2022. 64(3): p. e22252.

22. Blecharz-Klin, K., et al., Early paracetamol exposure decreases brain-derived neurotrophic factor (BDNF) in striatum and affects social behaviour and exploration in rats. Pharmacol Biochem Behav, 2018. 168: p. 25-32.

23. Hay-Schmidt, A., et al., Prenatal exposure to paracetamol/acetaminophen and precursor aniline impairs masculinisation of male brain and behaviour. Reproduction, 2017. 154(2): p. 145-152.

24. Baker, B.H., et al., Sex-specific neurobehavioral and prefrontal cortex gene expression alterations following developmental acetaminophen exposure in mice. Neurobiol Dis, 2023. 177: p. 105970.

25. Saad, A., et al., Is There a Causal Relation between Maternal Acetaminophen Administration and ADHD? PLoS One, 2016. 11(6): p. e0157380.

26. Graeca, M. and R. Kulesza, Impaired brainstem auditory evoked potentials after in utero exposure to high dose paracetamol exposure. Hear Res, 2024. 454: p. 109149.

27. Klein, R.M., et al., Gestational paracetamol exposure induces core behaviors of neurodevelopmental disorders in infant rats and modifies response to a cannabinoid agonist in females. Neurotoxicol Teratol, 2023. 99: p. 107279.

28. Klein, R.M., et al., Gestational exposure to paracetamol in rats induces neurofunctional alterations in the progeny. Neurotoxicol Teratol, 2020. 77: p. 106838.

29. Suda, N., et al., Therapeutic doses of paracetamol with co-administration of cysteine and mannitol during early development result in long term behavioral changes in laboratory rats. PLoS One, 2020. 16(6): p. e0253543.

30. Viberg, H., et al., Paracetamol (Acetaminophen) Administration During Neonatal Brain Development Affects Cognitive Function and Alters Its Analgesic and Anxiolytic Response in Adult Male Mice.Toxicological Sciences, 2013. 138(1): p. 139-147.

31. Philippot, G., et al., Adult neurobehavioral alterations in male and female mice following developmental exposure to paracetamol (acetaminophen): characterization of a critical period. J Appl Toxicol, 2017. 37(10): p. 1174-1181.

32. Dean, S.L., et al., Prostaglandin E2 is an endogenous modulator of cerebellar development and complex behavior during a sensitive postnatal period. Eur J Neurosci, 2012. 35(8): p. 1218-29.

33. Philippot, G., et al., Paracetamol (Acetaminophen) and its Effect on the Developing Mouse Brain.Front Toxicol, 2022. 4: p. 867748.

34. Kanno, S.I., et al., Glutathione peroxidase 3 is a protective factor against acetaminophen‑induced hepatotoxicity in vivo and in vitro. Int J Mol Med, 2017. 40(3): p. 748-754.

35. Rigobello, C., et al., Perinatal exposure to paracetamol: Dose and sex-dependent effects in behaviour and brain's oxidative stress markers in progeny. Behav Brain Res, 2021. 408: p. 113294.

36. Posadas, I., et al., Acetaminophen induces apoptosis in rat cortical neurons. PLoS One, 2010. 5(12): p. e15360.

37. Labba, N.-A., et al., Paracetamol perturbs neuronal arborization and disrupts the cytoskeletal proteins SPTBN1 and TUBB3 in both human and chicken in vitro models. Toxicology and Applied Pharmacology, 2022. 449: p. 116130.

38. Vigo, M.B., et al., Acute acetaminophen intoxication induces direct neurotoxicity in rats manifested as astrogliosis and decreased dopaminergic markers in brain areas associated with locomotor regulation.Biochemical Pharmacology, 2019. 170: p. 113662.

39. Schultz, S., et al., Effects of the analgesic acetaminophen (Paracetamol) and its para-aminophenol metabolite on viability of mouse-cultured cortical neurons. Basic Clin Pharmacol Toxicol, 2012. 110(2): p. 141-4.

40. Roberts, I.D., I. Krajbich, and B.M. Way, Acetaminophen influences social and economic trust.Scientific Reports, 2019. 9(1): p. 4060.

41. Dewall, C.N., et al., Acetaminophen reduces social pain: behavioral and neural evidence. Psychol Sci, 2010. 21(7): p. 931-7.

42. Freed, G.L., et al., Parental vaccine safety concerns in 2009. Pediatrics, 2010. 125(4): p. 654-9.

43. Bazzano, A., et al., Vaccine-related beliefs and practices of parents of children with autism spectrum disorders. Am J Intellect Dev Disabil, 2012. 117(3): p. 233-42.

Related articles:

Alternatives to Tylenol: Better, Safer Remedies
Tylenol: The Pain Reliever Class Action Lawsuits Need to Target Most
Let it Burn. It’s Good to Have a Fever. Here’s Why

About the author:

Jennifer Margulis, Ph.D., is an award-winning science writer and health journalist. The author/editor of eight books, she has worked on a child survival campaign in West Africa, appeared live on prime-time TV to champion an end to child slavery in Pakistan, and taught post-colonial literature to non-traditional students in inner city Atlanta. Support independent journalism and science writing by becoming a free or paid subscriber today. Or cut out the middleman by sending a one-time Venmo to @Jennifer-Margulis-2 (“1256”).