Acetaminophen (Tylenol) and the autism epidemic

reposted/revised from


The incidence of autism has risen 10-fold since the early 1980s, with most

of this rise not explainable by changing diagnostic criteria. Previc 2007 [1]

Compelling evidence implicating an environmental cause or trigger of autism must be the number of normally developing children who gradually or abruptly regress into autism between 12 and 18 months old. Parents implicated the diphtheria-pertussis-tetanus vaccine (DPT) in their child’s regression in reports to Bernard Rimland even before he founded the Autism Research Institute (ARI) in 1967 [2]. Rimland [3] suspected the “autism explosion” in the early 1980s was due to accelerated efforts by the Centers for Disease Control and Prevention (CDC) beginning 1978 [4] to encourage wider use of the measles-mumps-rubella vaccine (MMR). Yet the MMR, often implicated by parents in their child’s regression, never used the mercury-based preservative thimerosal the DPT and other vaccines formerly used (but does contain 10% glutamate from gelatin to preserve the viruses [5]).

Schultz and colleagues asked whether autistic regression after the MMR might be provoked, not by the vaccine itself, but by acetaminophen (Tylenol) given for its pain and fever. An online survey of parents revealed that children given acetaminophen for adverse reactions to the MMR were significantly more likely to become autistic than children given ibuprofen: “Children who used acetaminophen at age 12 to 18 months were more than eight times as likely to be in the AD [autistic disorder] group when all children were considered ... and more than 20 times as likely to be in the AD group when limiting cases to children with regression ....”[6] In a second paper Schultz [7] pointed out the synchronicity between the beginning of the autism epidemic and the CDC’s 1980 warning associating aspirin with Reye’s syndrome (based on Starko et al. 1980 [8]) – a rare but often fatal disease in children after a bout of flu or chicken pox. Schultz found the abrupt nationwide shift from aspirin to Tylenol that began in 1980 was associated with an increased number of California children with autistic disorders born after 1980.

This synchronicity Schultz detected is corroborated by Jon Pangborn’s assessment of the origins of the autism epidemic, based on thousands of cases reported to the ARI since the 1960s [9]. Pangborn, senior ARI biochemist for many years, noted that until about 1980, 50–60% of autistic children were autistic from birth, and 40–50% regressed into autism at about 18 months. “Around 1980,” Pangborn concluded, “all this began to change. The total frequency of occurrence doubled, doubled again, and by 1995 was approximately 10 times that of 1980. Furthermore, while the onset-at-birth type had increased 3 to 4 times, the onset-at-18-months type had skyrocketed to considerably more than 10 times its 1980 level.” Pangborn concluded that most of the autistic population now appeared to have “an acquired disease caused by something that we were not doing 20 years ago.”

Pediatrician James Orlowski and colleagues challenged the association of aspirin and Reye’s syndrome [10]. They argued: (1) salicylates like aspirin have alleviated fever and pain since the early 1900s, yet Reye’s syndrome was not reported until the early 1950s; (2) other studies worldwide showed no association between aspirin and Reye’s; (3) the incidence of Reye’s was already falling by 1979; (4) Reye’s virtually disappeared from countries that had not given children aspirin since the 1950s, as well as from countries that continued to give children aspirin; (5) U.S. Public Health Service studies between 1980 and 1987 corroborating a link between aspirin and Reye’s were seriously flawed.

My 2009 paper [11] emphasized the chronology of the autism epidemic and the toxicity of acetaminophen, a known liver poison. Schultz and colleagues noted young children detoxify acetaminophen via sulfation in the liver – a pathway known to be compromised in children with autistic disorders. I learned that during pregnancy the fetal adrenal gland sulfated the androgen/estrogen precursor dehydroepiandrosterone (DHEA) to its reservoir form DHEA sulfatemost common precursor of placental estrogens [12,13]. Did that explain the extreme male brain of autism recognized by Baron-Cohen and colleagues [14]? Furthermore, sulfation of DHEA required glutathione (GSH) as cofactor [15] – often low in these children.

Shaw recently presented compelling evidence confirming acetaminophen depletes glutathione – the body’s primary detoxifying agent and antioxidant, especially in the liver [16]. In a comprehensive indictment of Tylenol and its maker Johnson & Johnson, Shaw reported fresh evidence that emphatically implicates acetaminophen as a cause of the autism epidemic, most notably that Cuba – with an autism incidence a fraction of ours (1/300th) – requires vaccinations (especially against measles), prohibits over-the-counter Tylenol, and only rarely allows acetaminophen for vaccinations. Fevers persisting more than two days after vaccination are usually treated with prescription metamizole – a drug banned in the U.S. on questionable grounds.

The implications of this evidence are obvious – and staggering. All children in Cuba are vaccinated, especially against measles. Yet our autism rate is almost 300x theirs – mostly regressive autism about 18 months of age. We give Tylenol freely; Cuba requires a prescription because Tylenol is limited by the U.S. embargo. But perhaps Cuba uses a single measles vaccine; some think triple vaccines like the MMR and DPT induce regression. A measles vaccine was introduced into Cuba in 1971 [17]; the MMR introduced in 1986 [18]. If the MMR hasn’t provoked an epidemic of autism in Cuba since 1986, why would it do so in the U.S.? Another challenge: The MMR is usually given at 12–15 months; why does regression usually happen about 18 months? Schultz pointed out regression often develops gradually, over months. Acetaminophen given with vaccines, he suggested, may weaken a child’s immune system, so the child gets sick again and takes more acetaminophen, thus “slowly regressing into autism.”[19]

Shaw cited evidence implicating acetaminophen in many other disorders, notably the epidemic of asthma: “Depletion of GSH as a consequence of acetaminophen toxicity to the liver has attracted the most attention in the medical scientific community, as it can frequently be fatal or require a liver transplant or emergency treatment to prevent liver failure .... However, acetaminophen toxicity has been implicated in a wide range of other disorders in humans and/or experimental animals including cancer, birth defects, asthma, allergies, and brain toxicity.”[16]

Shaw noted recent evidence associating prenatal and perinatal paracetamol(acetaminophen in the UK) with autism. Bauer and Kriebel reported recommendations that paracetamol be given before and after circumcision: “These guidelines include the suggestion of a first dose ... two hours prior to the procedure, and doses every 4–6 hours for 24 hours following the procedure. Thus newborn males often receive 5–7 doses ...  during the developmentally vulnerable initial days of life.”[20] Another reason boys are 4x more vulnerable to autism than girls? Bauer and Kriebel also cited evidence that may explain the increased number of children born autistic: “In the early 1980’s about 42% of women used paracetamol during the first trimester of pregnancy. The rate climbed to over 65% in the early 1990’s, where it has essentially remained through 2004.”

Shaw reported that in recent years Johnson & Johnson has repeatedly run afoul of the Food and Drug Administration (FDA) – for mislabeling children’s products (increasing risk of overdose) and poor quality control and contamination at manufacturing plants; millions of bottles of children’s medicines containing acetaminophen have been recalled. Johnson & Johnson also makes Risperdal (risperidone), the antipsychotic drug for ASD with serious side effects.


1. Previc FH. Prenatal influences on brain dopamine and their relevance to the rising incidence of autism. Medical Hypotheses 2007;68:46–60.

2. Rimland B. The autism explosion. Autism Research Review International 1999;13(2):3–5. <>

3. Rimland B. The autism epidemic, vaccinations, and mercury. Journal of Nutritional & Environmental Medicine 2000;10:261–266.

4. Centers for Disease Control and Prevention. The Pink Book: Epidemiology and Prevention of Vaccine Preventable Diseases, 10th ed. 2008 <> [accessed 9/26/2009]

5. Hoernlein C. MSG and autism. <> [accessed 3/23/12]

6. Schultz ST, Klonoff-Cohen HS, Wingard DL, Akshoomoff NA, Macera CA, Ji M. Acetaminophen (paracetamol) use, measles-mumps-rubella vaccination, and autistic disorder: the results of a parent survey. Autism 2008;12(3):293–307.

7. Schultz ST. National Acetaminophen Sales and Autistic Disorder in California. (formerly at: <]> [accessed 9/26/09]  [reposted on this site]

8. Starko KM, Ray CG, Dominguez LB, Stromberg WL, Woodall DF. Reye’s syndrome and salicylate use. Pediatrics 1980;66(6):859–864.

9. Pangborn JB. Introduction to the diseases of autism and laboratory testing options. In: Pangborn JB, Baker SM. Biomedical Assessment Options for Children with Autism and Related Problems. San Diego: Autism Research Institute; 2002.

10. Orlowski JP, Hanhan UA, Fiallos MR. Is aspirin a cause of Reye’s syndrome? A case against. Drug Safety 2002;25:225–231.

11. Good P. Did acetaminophen provoke the autism epidemic? Alternative Medicine Review 2009;14(4):364–372. <>

12. Leowattana W. DHEA(S): the fountain of youth. Journal of the Medical Association of Thailand 2001;84:S605–S612.

13. Barker EV, Hume R, Hallas A, Coughtrie WH. Dehydroepiandrosterone sulfotransferase in the developing human fetus: quantitative biochemical and immunological characterization of the hepatic, renal, and adrenal enzymes. Endocrinology 1994;134:982–989.

14. Baron-Cohen S, Knickmeyer RC, Belmonte MK. Sex differences in the brain: implications for explaining autism. Science 2005;310:819–823.

15. Geier DA, Geier MR. A clinical and laboratory evaluation of methionine cycle-transsulfuration and androgen pathway markers in children with autistic disorders. Hormone research 2006;66:182–188.

16. Shaw W. Evidence that increased acetaminophen use in genetically vulnerable children appears to be a major cause of the epidemics of autism, attention deficit with hyperactivity, and asthma. Journal of Restorative Medicine 2013;2:1–16. <>

17. Galindo MA, Santín M, Resik S, Ribas MA, Guzmán M, Mas Lago P, et al. [Eradication of measles in Cuba]. [article in Spanish; English abstract] Revista Panamericana de Salud Pública 1998;4(3):171–177.

18. Reed G, Galindo MA. Cuba’s national immunization program. MEDICC Review 2007;9(1):5–7. <> [accessed 10/2/14]

19. Schultz S. Personal communication 2009.

20. Bauer AZ, Kriebel D. Prenatal and perinatal analgesic exposure and autism: an ecological link. Environmental Health 2013;12:41.