The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
Results of this study indicate that the association between acetaminophen use during pregnancy and neurodedevelopmental disorders is a non-causal association. Associations observed in models without sibling control may be attributable to confounding.
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Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
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If the mother is predisposed towards autism, then the child is also likely at a higher than average risk of autism based solely on genetics. But if a genetic predisposition also increases the likelihood that the mother might use Tylenol during pregnancy, which is entirely possible given that autism is related to sensory perception, which is in turn related to pain sensing, then it would appear as if acetaminophen use and the child's risk of autism were related, even though both associations might actually be explained by genetics.
So the authors examined sibling pairs that were discordant in acetaminophen exposure and found no significant difference in risk for autism between exposure and lack of exposure.
The associations reported from this Japanese cohort were similar to those in the Swedish study. In the general cohort, so unadjusting for siblings, prenatal exposure to acetaminophen was associated with a 6% uptick in autism rates. Recall in the Swedish study, it was 5%. But in the Japanese study, this did not reach statistical significance.
So over a median follow-up of about 13 1/2 years, the general cohort showed a very small but statistically significant positive association between prenatal acetaminophen exposure and autism. The hazard ratio is 1.05 and the confidence interval was 1.02 to 1.08. So what does that mean? That means it showed a 5% increase in relative risk.
But when they did the sibling analysis even this small trend towards an increased risk was completely abolished.
which is that once you correct for genetics and home environmental exposures, the risk of autism as it pertains to acetaminophen exposure is not causal.
So when they did that concordant discordant analysis, the correlation was entirely abolished. Um, when they compared and controlled for family environment and genetics as best as you could.
The absolute risk increase was 0.09% 09% increase at 10 years. So that's a that's a very small absolute risk increase less than onetenth of 1%.
In light of recent news, it's worth noting that the association between acetaminophen (e.g., Tylenol) use during pregnancy and childhood behavioral issues is not new.
In boys, exposure was also linked to autism spectrum disorder symptoms in a frequency-dependent manner.