If I understand your reply correctly, your conclusion is that epidemiologists should:
Discuss the mechanistic reasons re: the direction of IQ <-> Alcohol consumption and
Especially distrust mendelian randomization studies where (1.) isn’t strongly argued for, and which get really large estimates.
I think these are important points!
Yep!
But given the very small effects estimated here, you aren’t arguing for a change to the interpretation of the studies in the post, right? :-)
In principle, this sort of problem can also lead to smaller effects, but it’s probably less likely, so it might be fine? I mean it’s possible I’ve missed something that could make it a problem.
Looking closer, the ADH1B that the variant is in is involved in alcohol metabolism, so that probably gives a plausible idea of how the MR mechanism would work.
Discuss the mechanistic reasons re: the direction of IQ <-> Alcohol consumption and
Actually I wanna issue a correction here. They should discuss the mechanistic reasons for the SNP → alcohol consumption link. The point of MR is to figure out things about the IQ <-> alcohol consumption causal link without necessarily having good mechanistic knowledge of it. But as Pearl says, if you put no causes in, you get no causes out; in exchange for the IQ <-> alcohol consumption causal link, you must know even more details about the effects of the SNP that you use for estimation.
Martin here, the main author of the above. Thanks a ton for this!
If I understand your reply correctly, your conclusion is that epidemiologists should:
Discuss the mechanistic reasons re: the direction of IQ <-> Alcohol consumption and
Especially distrust mendelian randomization studies where (1.) isn’t strongly argued for, and which get really large estimates.
I think these are important points!
But given the very small effects estimated here, you aren’t arguing for a change to the interpretation of the studies in the post, right? :-)
Yep!
In principle, this sort of problem can also lead to smaller effects, but it’s probably less likely, so it might be fine? I mean it’s possible I’ve missed something that could make it a problem.
Looking closer, the ADH1B that the variant is in is involved in alcohol metabolism, so that probably gives a plausible idea of how the MR mechanism would work.
Actually I wanna issue a correction here. They should discuss the mechanistic reasons for the SNP → alcohol consumption link. The point of MR is to figure out things about the IQ <-> alcohol consumption causal link without necessarily having good mechanistic knowledge of it. But as Pearl says, if you put no causes in, you get no causes out; in exchange for the IQ <-> alcohol consumption causal link, you must know even more details about the effects of the SNP that you use for estimation.