Today I was going to try to explain why I think it’s ok to take pseudoephedrine (i.e. Sudafed, the good cold medicine) during pregnancy, but I got really wrapped up in explaining details and nuances of my reasoning, and then I got sidetracked into American attitudes towards pregnancy and risk, and risk communication in general, and it’s all just too much to tackle in a single post without making most people’s eyes glaze over immediately.
I still want to try, but I think I’ll have to limit my explanation, and then follow up with more detail in another post. I’m thinking of how one of my favorite professors designed his curriculum – he liked to say that on the first day of class, he taught the entire course. Then on the subsequent two days, he covered the entire course again, but in double the detail. And so on, with the subsequent three days, etc. Only I’m pretty sure I’ll get distracted by something before I can get that far, so don’t bother unsubscribing from my blog if you find this boring and irrelevant.
OK, so the short version:
The scientific evidence of correlation* between pseudoephedrine use and incidence of birth defects or other negative outcomes** is not compelling to me, and therefore I have no problem taking it when I myself am pregnant.
A few studies did not find any correlation, and a few studies found a correlation for pseudoephedrine only when combined with other drugs (e.g., in NyQuil). The studies that found a correlation were case-control studies, and they found that the odds of the occurrence of negative outcomes were roughly doubled when compared to controls.
There are two big reasons I do not put a lot of stock in this finding:
1. Because the correlation was only observed for combination products, it means that IF there is a causative effect, it is due to an interaction between pseudoephedrine and whatever it was combined with, OR the correlation is due to confounding factors or random chance (source). The latter are more likely, in my scientific opinion.
2. Case-control studies are one of the least compelling kinds of epidemiological studies. They are useful in situations where the outcomes of interest are very low incidence, as is the case here (the incidence is about 0.047% of births), but because of their design, they are heavily influenced by confounders. They are better than anecdata, certainly, but aren’t considered to carry much weight of evidence.
Further, the sensitive window for the negative outcomes is in the first trimester, and more likely in the first eight weeks of gestation, during organogenesis. It is estimated that 8-12% of pregnant women in the U.S. take pseudoephedrine during this window. Despite that high level of exposure, epidemiological studies haven’t been able to find a clear cut correlation. Even for the combination products, it strikes me as pretty hazy at best.
Ultimately, this just doesn’t meet my personal threshold for worrying about something. If we can’t detect an obvious correlation to an effect at a population level, I can’t get worked up about it. The background incidences of these negative outcomes are quite low. The possible additional risk – as estimated by the least compelling kind of epidemiological study – is still quite low. That possible additional risk is limited to combination products, which I tend to avoid anyways (different subject for a different day), and to the first trimester. So even if I were inclined to place stock in the case control study findings, that would only keep me from taking NyQuil before twelve weeks – and more likely, just before eight.
**The negative outcomes in question are gastroschisis, small intestinal atresia, and hemifacial microsomia.