An article in the New York Times this week warns that prenatal use of acetaminophen—the main ingredient in Tylenol—has been linked to an increased risk of asthma and attention disorders in children whose mothers took the drug.
Acetaminophen is found in over 600 over-the-counter and prescription medications. Petra Arck, professor of fetal-maternal medicine at the University Medical Center Hamburg-Eppendorf, whose rodent experiments have found that acetaminophen stresses the liver and alters the placenta in pregnant mice, told the Times that because it’s so common pregnant women may be taking more acetaminophen than they are aware.
The damage done by acetaminophen seems to be dose dependent—the more a pregnant woman takes, the more serious the effects in her offspring. But since it’s found in so many products, many marketed for babies and children, what if infants, too, are being exposed to damagingly high levels of acetaminophen?
If acetaminophen can harm the fetus during pregnancy, when the baby has the protection of the mother’s liver, as well as the placenta, what if it’s even more harmful when given directly to infants?
New science has raised troubling concerns about the safety of acetaminophen, the main ingredient in Tylenol, which is nonetheless marketed for pain and fever relief in infants. This photo was taken at a Toys R Us in North Carolina.
The increasing popularity of acetaminophen to treat fever and pain in small children began in the 1980s after it was discovered that aspirin might cause Reye syndrome, a rare but sometimes fatal disorder that causes seizures, liver swelling, and brain swelling. The concern over Reye syndrome back then seemed to justify halting the use of aspirin. But now there is a growing body of scientific evidence suggesting that we inadvertently replaced aspirin with something more dangerous.
In 2008 a team of researchers from UCSD and San Diego State, headed by Stephen Schultz, Ph.D., conducted a survey that found a 20-fold increase in the risk of brain disorders with use of acetaminophen after vaccination, but not with ibuprofen.
Taken out of context, the Schultz study was not enough to sound an alarm. It relied on participants’ recall and did not include independent verification of the amount of acetaminophen toddlers had been given. Another strike against it was that the study size was small (83 brain damaged children and 80 controls). But when you look at subsequent science that supports Schultz’s results, it becomes harder to understand why the medical community has generally ignored the possible harms of acetaminophen to children.
Indeed, a much larger study, involving more than 205,000 children, also published in 2008 (this time in The Lancet) found use of acetaminophen in the first year of life was associated with inflammatory diseases, including asthma and eczema by age six and seven.
Then in 2010, Schultz and Kevin Becker, Ph.D., who trained at Johns Hopkins in Molecular Biology and Genetics and is currently head of a research unit at the National Institutes of Health, hypothesized that the use of acetaminophen in early childhood “may significantly alter subtle immune processes,” and be a possible cause of both asthma and brain dysfunction.
William Shaw, Ph.D., a clinical chemist who had previously worked for the Centers for Disease Control, provides a detailed explanation of how acetaminophen causes damage: acetaminophen depletes the body’s supply of glutathione. Since glutathione is a molecule essential for clearing toxins, the use of acetaminophen can result in essentially a toxic wash of the brain during development.
Scientists now understand even more: acetaminophen derails something called DNA methylation, which is vital in the developmental biology of most life as we know it, from bacteria to humans. Unless you are a single-celled yeast or a tiny roundworm, two organisms that don’t use DNA methylation to control development, acetaminophen can disrupt an essential biological process, one that you need to have a healthy brain and body.