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Schultz et al (2008) raised the question whether regression into autism is triggered, not by the measles-mumps-rubella vaccine (MMR), but by acetaminophen (TylenolA®) given for its fever and pain.
In the May 2008 issue of the journal Autism, Schultz et al reported an association between autism and acetaminophen (paracetamol, TylenolA®) given children for fever, pain, and other adverse reactions to the measles-mumps-rubella vaccine (MMR), usually administered between 12 and 15 months of age.
Although distribution studies detected no association, the MMR has long been suspected of provoking autism, especially by parents whose seemingly normal child regressed into autism not long after receiving the vaccine [2-4]. Interestingly, no parent in the survey reported giving aspirin after a childa€™s MMR vaccination.
Orlowski et al offered compelling arguments, however, that aspirin was not the cause of Reyea€™s syndrome. The most compelling evidence linking acetaminophen use and autism is their rapid synchronous rise in recent decades.
Pangborna€™s conclusions were based on thousands of cases collected by the Autism Research Institute (ARI) since the 1960s (Figure 1) [2-4]. Schultz compared the nationwide shift from aspirin to acetaminophen against the number of children with autistic disorders eligible for services in California born before and after 1980. Schultz adapted his graph from a 1999 graph by Californiaa€™s Department of Developmental Services (DDS), which depicted a steep rise in the number of California children with autistic disorders born after 1980 [13].
Because infanta€™s Tylenol is three times more concentrated than childrena€™s Tylenol [15] and parents may not realize childrena€™s cold remedies often contain acetaminophen, acetaminophen overdose in young children is not uncommon[16,17]. Parents and autism support groups commonly report that autistic episodes are triggered when these children eat wheat, corn, sugar, apples, bananas, chocolate, cheese, and other dairy products [21]. Oa€™Reilly and Waring studied 40 autistic children intolerant of certain foods and chemicals.
Alberti et al subsequently used acetaminophen to probe the relative contributions of the sulfate and glucuronide pathways of excretion in low-functioning children with autism. Pangborn measured plasma amino acids in 32 children with autism, detecting marginal to subnormal levels of cystine (two cysteine molecules linked by sulfhydryl groups) in 60 percent. One critical sulfation reaction during pregnancy converts the adrenal androgen and estrogen precursor dehydroepiandrosterone (DHEA) to its sulfate DHEAS, a storage or reservoir form of DHEA [26] that takes 15 times longer to clear from the blood [27].
Mothers of autistic children commonly suffer more bacterial and viral infections [33] and fevers [6] during pregnancy, for which they commonly take acetaminophen [34]. Acetaminophen impairing sulfation before and after birth may explain why children with autism have smaller brains at birth (estrogen deficiency) then an accelerated and prolonged growth spurt of male-specific brain structures within a few months of birth (androgen excess).[37,38] The testosterone-dependent amygdalae are larger than normal in these children and the estrogen-dependent corpus callosum disproportionately smaller [38,39]. Other good sources of sulfur are cabbage, onions, garlic, dried fruit [42] oral supplements like whey protein [23] and methylsulfonylmethane (MSM) [43] and a high-protein diet. Giving aspirin to children with autism, however, may tax the liver as much as acetaminophen, although salicylates are usually metabolized as glucuronides [46]. The synchronicity Schultz detected between the onset of the autism epidemic and the surge in acetaminophen use after the CDCa€™s 1980 warning against aspirin seems unlikely to be artifact or coincidence. For autism, the critical distinction between aspirin and acetaminophen may be the difference between aggravation and provocation.
Considerable evidence supports this contention, most notably the exponential rise in the incidence of autism since 1980, when acetaminophen began to replace aspirin for infants and young children.
Children given acetaminophen after the MMR were significantly more likely to become autistic than children given ibuprofen [1]. Schultz et al, however, raised the intriguing question whether the trigger for autism is not the MMR itself, but acetaminophen given for its fever and pain. This may reflect awareness that aspirin is no longer considered safe for infants and young children, after being implicated in Reyea€™s syndrome (liver and brain damage after viral infection) in the 1980s.
Although salicylates like aspirin have been used to alleviate fever and pain since the beginning of the 20th century, Reyea€™s syndrome was not reported until the early 1950s. When Rimland founded the ARI in 1967, parents were already reporting their child deteriorated into autism soon after the diphtheria-pertussis-tetanus vaccine (DPT) [2,3].
Decreased nationwide sales of childrena€™s aspirin and increased sales of childrena€™s acetaminophen products beginning about 1980 were associated with an increased number of California children with autistic disorders born after 1980.
Schultz et al noted that sulfation by the liver is the primary pathway to detoxify and excrete acetaminophen in children younger than 10 [1]. All had very low levels of phenolsulfotransferase (PST), an enzyme that sulfates phenols and amines for excretion.
They too found these children were less able than normal children to sulfate phenols and amines, and suggested this might lead to accumulations of unmetabolized catecholamine neurotransmitters (dopamine, norepinephrine, and epinephrine) in the brain, with neurotoxic effects [21].
DHEAS from the fetal adrenal cortex is the most common precursor of the placental estrogens so vital to fetal growth and maturation [28]. If their babies are born cysteine-deficient, newborn boys may be more vulnerable because their uptake of cysteine takes longer to mature [35]. Oral magnesium sulfate, which is poorly absorbed, draws water into the intestines, potentially causing diarrhea; well-absorbed magnesium taurate provides magnesium as well as sulfur from taurine [40].
Alberti et al noted that salicylates are primary biochemical offenders in autistic children, and high dose aspirin inhibits the sulfating enzyme PST [21]. Cox and McDowell challenged the methods Schultz et al used to gather participants and controls for the online survey, arguing they were biased and insufficiently random, and no estimate of sample size was given. Could the epidemic of autistic regression be due to factors in the MMR vaccine itself (e.g. If replacing aspirin with acetaminophen provoked the autism epidemic, why is its prevalence in the United States comparable to its prevalence in France [55], where children continued to receive aspirin throughout the Reyea€™s epidemic?
If the MMR is usually given at 12-15 months, why does autistic regression usually occur at about 18 months? Yet can it be ethical to administer acetaminophen to a child whose ability to detoxify acetaminophen may be critically impaired? The Autism Research Institute also concluded that autism rates began to multiply around 1980, especially regression after the MMR. Although aspirin and other salicylates can worsen behavior in children already autistic, they have not been implicated in autistic regression in previously normal children.


The impetus for this shift a€“ a Centers for Disease Control and Prevention warning that aspirin was associated with Reyea€™s syndrome a€“ has since been compellingly debunked. An online survey of parents yielded 83 children with autism and 80 control children ages 1-18 years. Because Reyea€™s syndrome virtually disappeared worldwide after aspirin was replaced by other antipyretics and analgesics during the 1980s, parents, pediatricians, and hospitals today commonly give infants and young children acetaminophen or ibuprofen for fever and pain. Furthermore, Reyea€™s syndrome disappeared from countries like Australia that had not given aspirin to children since the 1950s, as well as from countries like France and Belgium that continued to give aspirin throughout the 1970s, 80s, and 90s. Rimland suspected the increase in autistic regression at 18 months was due to wider use of the MMR vaccine a€“ part of an accelerated effort to eradicate measles that began in 1978 [7]. Schultz also found that certain critical events in the history of acetaminophen use were soon followed by inflections in autism rates. To probe the sulfation pathway they administered 500 mg acetaminophen to these children, then collected urine over the next eight hours. Kidd concluded these studies by Waring et al amount to a€?direct proof a€? that children with autism are less able to sulfate foreign and native phenols and amines [19].
Pangborn noted, however, that Waring found higher than normal levels of plasma cysteine in children with autism, as well as higher ratios of cysteine to sulfate (suggesting a cysteine utilization disorder), and after administering paracetamol (acetaminophen), lower than normal levels of paracetamol sulfate. The Feingold Association has received parent reports of significant improvements in behavior of autistic children after removing gluten (wheat) and casein (dairy) products from their diets, as well as salicylates naturally present in fruits and vegetables.
These writers also suspected parents might not accurately recall years after the MMR vaccine whether their child was given acetaminophen [48]. Deligne et al reported that in 2003, 90 percent of more than 500,000 prescriptions for fever in French infants less than three months old were written for paracetamol (acetaminophen) [56]. One alternative: when parents become sufficiently wary of giving acetaminophen to infants and young children, the same kind of a€?natural studya€? may occur as when acetaminophen replaced aspirin in the 1980s [9]. Schultz et al found that children given acetaminophen for reactions to the MMR were more likely to become autistic than children given ibuprofen.
Acetaminophen (paracetamol) use, measles-mumps-rubella vaccination, and autistic disorder: the results of a parent survey. Prenatal influences on brain dopamine and their relevance to the rising incidence of autism. Metabolic endophenotype and related genotypes are associated with oxidative stress in children with autism.
Dehydroepiandrosterone sulfotransferase in the developing human fetus: quantitative biochemical and immunological characterization of the hepatic, renal, and adrenal enzymes. A clinical and laboratory evaluation of methionine cycle-transsulfuration and androgen pathway markers in children with autistic disorders.
Dehydroepiandrosterone and dehydroepiandrosterone sulfate production in the human adrenal during development and aging. Faulty serotonin a€“ DHEA interactions in autism: results of the 5-hydroxytryptophan challenge test. The time of prenatal immune challenge determines the specificity of inflammation-mediated brain and behavioral pathology. Localization of white matter volume increase in autism and developmental language disorder. Thimerosal neurotoxicity is associated with glutathione depletion: protection with glutathione precursors. Continuing increases in autism reported to Californiaa€™s developmental services system: mercury in retrograde. If aspirin is not to be feared as a cause of Reyea€™s syndrome, and acetaminophen is to be feared as a cause of autism, can the autism epidemic be reversed by replacing acetaminophen with aspirin or other remedies? Children with autism had more adverse reactions to the MMR and were more likely to have been given acetaminophen than ibuprofen for those reactions. On the other hand, the 1980s was also the decade when acetaminophen largely replaced aspirin for infants and young children. The liver uses sulfate derived from the amino acid cysteine to make soluble for excretion a variety of foreign and domestic substances.[19] The liver also uses cysteine to synthesize the antitoxin and antioxidant glutathione [22] as well as metallothionein, which transports zinc and copper and binds mercury and other toxic metals [23]. Most children had reduced urine output over the eight hours and were feverish and a€?generally off-colour.a€? The researchers warned about this effect of acetaminophen in these children, given relatively freely for minor illness [24]. They noted that DHEA can convert to androstenedione and then testosterone, or be sulfated to the a€?normally favored storage moleculea€? DHEAS. Pangborn warned that a sudden influx of cysteine may mobilize toxins the body is not ready or able to excrete [4]. Director Hersey concluded: a€?I cannot say if aspirin causes more problems than acetaminophen for autistic kids. Schultz replied that asking parents of autistic children to have their friends with normal children take the survey was an excellent way to select controls, because they represented the population studied, yet did not have autism.
Dales et al calculated that the incidence of autism in California children born from 1980 onward increased more rapidly than the use of the MMR vaccine [50]. Acetaminophen given for the vaccine, he suggests, may weaken a childa€™s immune system, so the child gets sick again and takes more acetaminophen, thus a€?slowly regressing into autism.a€?[57] This scenario may also apply to acetaminophen poisoning the liver. When enough parents stop giving (and taking) acetaminophen, and give aspirin or another remedy instead, any effect on the incidence of autism may be apparent within several years.
Because acetaminophen suppresses the immune system as well as depletes the livera€™s supplies of detoxifying agents, the question remains open which pathology is more decisive. Compared to controls, children ages 1-5 years with autism were eight times more likely to have gotten sick after the MMR vaccine, and were six times more likely to have taken acetaminophen. Public Health Service studies between 1980 and 1987 that associated aspirin with Reyea€™s syndrome, Orlowski et al found serious problems in all a€“ even doubt the researchers were actually studying Reyea€™s.
California children born in 1977 were less likely to be diagnosed with autism than children born in previous years. James et al detected significantly reduced plasma levels of methionine, cysteine, and glutathione and reduced methylation capacity in 80 children with autism; plasma cysteine was severely reduced in more than 65 percent [25].


Because sulfation of DHEA requires glutathione as cofactor, they proposed that glutathione deficiency in these children causes less DHEA to convert to DHEAS and more to androstenedione and testosterone [29]. When acetaminophen overdose depletes the livera€™s supplies of sulfate and glutathione and toxicity develops, the current treatment is N-acetylcysteine to replenish intracellular glutathione [44]. The reason why we suggest acetaminophen in place of aspirin is because aspirin is a a€?salicylatea€™ and a known troublemaker for many people. The original paper by Schultz et al pointed out several reasons the population of autistic children in the survey might not have been random [1].
By depleting sulfate, glutathione, and metallothionein, acetaminophen may make a child more vulnerable to a variety of substances, even the phenolic amines and salicylates in food. Immune suppression inducing more illness thus more acetaminophen may eventually result in toxic levels. Children with autism who regressed in development were four times more likely to have taken acetaminophen after the vaccine.
They noted other studies worldwide that showed no association between aspirin and Reyea€™s syndrome. Public Health Service and its Centers for Disease Control and Prevention (CDC) reported that aspirin was associated with Reyea€™s syndrome [8] a€“ a rare but often fatal disease in young children after a bout of flu or chicken pox. In autumn of 1982 seven people died after ingesting Tylenol capsules laced with cyanide; in 1986 one person died after ingesting Tylenol capsules similarly tampered with. A similar shift of adrenal steroid synthesis occurs in mother and fetus during complications of pregnancy, and in adults under stress, increasing cortisol at the expense of DHEAS [30]. Kidd concluded N-acetylcysteine and oral glutathione were safer than oral cysteine, and noted ascorbate (vitamin C) may protect against glutathione depletion [22].
Schultza€™s reply also noted that the effects of acetaminophen were so great they were significant even for the relatively small sample. In any case, greater use of the MMR does not explain three times more cases of autism present at birth. Reddening of the face and ears (a common response to trigger foods) may be mistaken for fever, prompting more acetaminophen, which eventually reaches toxic levels.
Impaired sulfation of DHEA and testosterone before and after birth may explain the extreme male brain.
If aspirin is not to be feared as a cause of Reyea€™s syndrome, and acetaminophen is to be feared as a cause of autism, the most direct countermeasure may be low-dose aspirin to relieve pain and high fever in infants and young children (and mothers during pregnancy).
Illnesses concurrent with the MMR were nine times more likely in autistic children when all cases were considered, and 17 times more likely after limiting cases to children who regressed [1]. As for the argument that Reyea€™s disappeared after aspirin use declined in infants and young children, Orlowski et al showed that the incidence of Reyea€™s syndrome was already falling by 1979 [5].
The impact of these studies on the publica€™s perception of aspirin for children was dramatic [9] a€“ perhaps abetted by the makers and vendors of acetaminophen [10]. These events precipitated sharp declines in nationwide sales of acetaminophen, accompanied by declines in the numbers of California children with autistic disorders born in 1984 and 1987 (Figure 2) [12].
Strous et al found plasma DHEAS significantly low in adults with autistic spectrum disorders [31]. Because molybdenum supplements improved behavior in 14 of 38 autistic children [42] further investigations seem warranted.
To minimize recall bias they had analyzed a smaller group of children ages 1-5 years, thinking parents of younger children would better remember whether their child was given acetaminophen after the MMR vaccine.
The mercury-containing preservative thimerosal in vaccines also depletes glutathione [51] but thimerosal was never a component of the MMR vaccine [52].
Fever and abdominal pain from unsuspected liver damage are commonly treated with acetaminophen [16].
If acetaminophen provokes autistic regression after vaccines, parents have less reason to fear vaccines.
The impact of these studies on the publica€™s perception of aspirin for children was dramatic [9] a€“ perhaps abetted by the makers and vendors of acetaminophen [10].A  Arrowsmith et al compared nationwide sales of aspirin and acetaminophen during that time, finding sharp decreases in the purchase and use of childrena€™s aspirin between 1980 and 1985 and a reciprocal increase in sales of childrena€™s acetaminophen products [11]. Croonenberghs et al detected a high ratio of plasma cortisol to DHEAS in autistic adolescents [32]. Torres recommended that fever suppressants be reserved for severe fevers in young children, on grounds that fever helps mature the immune system [34]. The association of autism with acetaminophen was highly significant even for this smaller group [49]. Furthermore, the incidence of autism continues to rise even though thimerosal is no longer used to preserve most pediatric vaccines [53]. Sulfation is also important for the excretion of steroids, including DHEA and testosterone [4,19].
Large trials have shown that low-dose aspirin during pregnancy is relatively safe for mother and child [45].
Many of our members use various homeopathic remedies a€“ theya€™re a very good option since they dona€™t contain unwanted additives such as artificial dyes and flavorings. On the other hand, in some states children still receive thimerosal-preserved vaccines [54]. Another choice would be to ask a compounding pharmacist to make up a product to fit the childa€™s needs. Haley also noted the oxidation of sulfite to sulfate requires a molybdenum cofactor inhibited by mercury [54] .Urinary sulfite is high in autistic children, and molybdenum supplements improved clinical symptoms [42].



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