[ben30]

Fair point on the "ended debate" phrasing - that was imprecise on my part. What I should have said is "the Swedish study provides the strongest evidence to date and shifts the burden of proof." It's not actually a single study though. The pattern is consistent across study quality levels:

Population studies (many): Small associations, but can't control for confounding

Negative control studies (several): Associations weaken when using better controls

Sibling studies (multiple, including Swedish): Associations disappear entirely

Meanwhile, fever studies (dozens): Consistent risk signals across different populations

The Swedish study is just the largest and best-designed in a hierarchy of evidence that all points the same direction. When you see this "dose-response by study quality" pattern - where better methodology consistently yields weaker effects - it's usually a strong signal that the original association was artifactual.

The Economist piece published yesterday reinforces this. They mention the NIH study of 200,000 children that "found no link at all" - that's another high-quality study reaching the same conclusion. Meanwhile, the studies showing associations (Nurses' Health Study II, Boston Birth Cohort) are exactly the type of population studies that can't control for the fever/infection confounding.

Science is never "settled" in an absolute sense, but the weight of evidence here is pretty clear. We're not waiting for more acetaminophen studies - we're ignoring the ones we already have while making policy based on weaker evidence.

That's the real problem with the current policy shift.

[Ancapistani]

> Fair point on the "ended debate" phrasing - that was imprecise on my part.

Oh, no worries. I was fairly certain I understood what you meant. Honestly that part of my comment was intended for others reading it, as it certainly seems that many people do believe a single peer-reviewed study should end the debate.

> the Swedish study provides the strongest evidence to date and shifts the burden of proof

100% agree :)

> It's not actually a single study though.

Unless I'm missing something, it is. It looks at a single population (Swedish children born between 1995 and 2019) that is divided into multiple cohorts. This approach strikes me as entirely valid -- but it also weakens the strength of the signal that it provides. With a population of this size and number of recorded attributes, there are likely cohorts that could be found to support any hypothesis the author would like. There are almost certainly many that would meet the bar of statistical significance if you're willing to form the hypothesis based on the data.

In other words, my initial impression is that it's potentially a variant of "P-hacking", regardless of intent. Unless the hypothesis was formed a priori, recorded, and not modified the results are evidence that a pattern may exist but not proof that it does.

> The Swedish study is just the largest and best-designed in a hierarchy of evidence that all points the same direction

From my perspective -- and to be clear, that's very much a lay perspective! -- I agree, and that direction is "there is likely a correlation between the use of acetaminophen during pregnancy and childhood autism diagnosis".

... but at the risk of being tiresome, correlation is not causation. My (unproven!) hypothesis at this point is that both higher rates of autism and acetaminophen use are a result of persistent fevers, which itself is likely a result of chronic systemic inflammation.

If that is in fact the case, then it would simultaneously be true that acetaminophen use would be a strong leading indicator of autism and that ceasing the use of acetaminophen during pregnancy would actually _increase_ the rate of autism overall.