Yes, Prenatal Acetaminophen Use Can Cause Autism, but let's quit ignoring the elephant in the living room...
by Brian Hooker, PhD, Chief Scientific Officer of Children's Health Defense
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Yes, Prenatal Acetaminophen Use Can Cause Autism, but let's quit ignoring the elephant in the living room...
Brian Hooker, PhD
Chief Scientific Officer of Children's Health Defense
The Washington Post and Politico have both reported that today the White House and HHS Secretary are going to announce that acetaminophen during pregnancy is a causal factor in the autism epidemic, as autism prevalence in the US has exploded since the late 1980s/early 1990s. I suspect that the question will not be left there and seriously hope that we can stop avoiding the elephant in the living room, infant vaccines.
Vaccines and vaccine components have been shown to be directly related to the explosion of autism cases in the US since the late 1980s by many independent studies. In research comparing vaccinated versus unvaccinated children, Mawson et al. as well as Hooker et al.show autism rates at least four times higher in the vaccinated group. The relationship between thimerosal exposure through vaccines and autism incidence has also been affirmed by many studies. Aluminum adjuvant exposure and MMR vaccine uptake have also been linked to the autism epidemic.
Interestingly, despite the fact that a CDC website still proclaims, "Vaccines don't cause autism," CDC scientists have studied only the MMR vaccine and thimerosal in vaccines in relation to the autism epidemic. Both studies (DeStefano et al. 2004 for the MMR vaccine and Vestraeten et al. 2003 for thimerosal exposure via vaccines) involve multiple iterations of analyses designed to cause existing, statistically significant relationships to "vanish." Both also employ standard CDC epidemiology trickery such as eliminating the zero exposure control group or limiting the size of the cohort to reduce statistical power to find an association.
Despite these near Olympian epidemiologic maneuvers, the DeStefano et al. paper could not get rid of a highly significant 67% increase in autism in boys who received the MMR on time versus those who delayed the jab until after 3 years of age. Similarly, the Verstraeten et al. study, with its five separate iterations, was still a "neutral study" according to the lead investigator, Dr. Thomas Verstraeten and couldn't rule out a relationship between thimerosal exposure and autism.
But, let's ignore that elephant for a bit longer and talk about the problems regarding prenatal Tylenol use and autism causation...
First, the prenatal acetaminophen exposure window is likely the least problematic compared to perinatal and the postnatal development periods. When a pregnant woman takes acetaminophen, she most probably has proper detoxification pathways that can eliminate the majority of the medication, lifting the toxicity burden off of the developing unborn child. Even if the woman has impaired glutathione-based detoxification, she could instead detoxify acetaminophen through the alternative beta-glucuronidase pathway which is severely reduced in the first months of life. Will the unborn child still suffer the effects of acetaminophen toxicity? Yes, under the right conditions, but the unborn child is still largely protected by its mother.
The perinatal exposure window, including labor and delivery as well as the rest of the hospital stay for the newborn (and, many times in the case of males, circumcision), is the absolute worst interval to receive acetaminophen. In this period of infant rapid development, toxicity is borne by the infant alone as the infant's bloodstream is now separate from that of the mother. If the baby has limited glutathione reserves due to impaired methylation and sulfation pathways or increased oxidative stress via vaccines, vaccine components, glyphosate, heavy metal contaminants, genetics, etc., then they will not properly detoxify acetaminophen, leading to brain exposure of the toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI).
This phenomenon can occur up to the sixth birthday, when the brain appears to be sufficiently developed so that the induction of autism becomes extremely rare. However, as I indicated above, the perinatal exposure window, as opposed to postnatal, is the worst time period that an infant could receive acetaminophen. Within this timeframe, the infant is indeed smaller (with less blood volume) causing the overall exposure concentration to be higher in the infant's bloodstream. A study comparing cord blood acetaminophen levels in neonates, indicated a 3.6-fold increase in subsequent autism diagnoses in the children within the upper third as compared to the children in the lower third. In addition, a 2015 study from Denmark showed that circumcised boys were 2 times as likely to develop autism prior to 5 years of age as compared to uncircumcised boys. Here, circumcision is used as a "surrogate procedure" for acetaminophen use, presumably for pain relief following the procedure. However, the authors indicate that they "had no data available" on analgesics use after the procedure.
Also, even if acetaminophen is necessary for autism to develop, it is not fully sufficient to cause the disorder alone. The research clearly points to an oxidative stress component or components that differentiate between infants who develop autism after acetaminophen exposure versus those infants who do not.
This leaves a hole big enough for a Mack truck to drive through regarding the other factors that are involved in autism causation, especially that pesky elephant, vaccines. Let's not leave out environmental contaminants such as pesticides, herbicides and heavy metals, infection during pregnancy causing maternal immune activation, genetic components related to impaired detoxification and many others. My hope and confidence are that Secretary Kennedy will continue to research vaccines as well as these other factors and leave no stone unturned regarding autism causation.
By the way, please don't just tell us to avoid acetaminophen if we're pregnant, give us a bottle of folinic acid (i.e., leucovorin) capsules, pat us on the head and send us on our merry way... Our children deserve much better.
by Brian Hooker, PhD, Chief Scientific Officer of Children's Health Defense
For additional reading on the topic, consult the GreenMedInfo.com autism spectrum disorder database, and my recent articles on Tylenol below.
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
This is Part III in our series…







What about ultrasounds early in the pregnancy, especially the high definition ones. Is it possible that the ultrasound waves have an effect on the delicate and developing brain? I suspect there are multiple causes. We need to accurately assess all potential causes.
Oh geeez.... who correctly called this week's ago? It's astonishing that they are playing this card. This feels like completely mockery at this point.