This was the most difficult diavlog of the seven I've done so far. 60 minutes just wasn't enough for this conversation and I had to do a lot of on-the-fly judgment of what I should elaborate on, and what I should simplify or elide for the sake of concision. The others were more "interview" formats where there was a more formal structure, as opposed to riffs. Also, Eliezer and a subset of the audience knows a fair amount of biology, but the majority of the audience did not, so I kept having to navigate between these two tensions.
I assume Eliezer had similar issues when we got the section where Kahneman & Tversky's ouvre were implicit background assumptions, but we'd burned through 2/3 of the time by then so the choice on whether to elucidate or not was made for him :-)
This was a survey of ancestry/genetic structure. Not trait values. Here is the post, just page down to the image and you can see why they were interested:
Right. I'm gonna have to find a balance between using bio-words and stuff I translate into normal speak on-the-fly. My first thought was to blurt out trisomy 21, and then I would have had to use the word non-disjunction. So I simply noted it was a problem with chrom 21 , and that is the smallest chrom so as to minimize dosage dependent effects.
Looking at your comment I am not sure we disagree. Rather than unpacking what I'm trying to get at (which is orthogonal to the discussion), I'll leave it be. But if you are curious look up "heritabitility" in Hartl & Clark, they explain the issues more lucidly than I could here.
Right. Though below Tim notes one truism: on a continuous trait with a non-trivial heritability (IQ) you likely don't have strong long-term unidirectional fitness implications. Otherwise, all the genic variance would be gone (strong selection + high heritability).
Oh, and for the record, I think IQ variance is a moderately-to-highly heritable trait. I'm arguing about genetic architecture here, not whether variance is due to genes or not (I think a large proportion is).
"Actual evidence from Razib would, of course, have dominated other considerations."
To make the evidence compact I'd have to produce some charts showing that when a new large effect QTL is published there's often a media blitz (perhaps via # of articles published as a function of time), but that as time passes the finding is not validated by subsequent researchers using a wider set of populations. As it is, what I have is personal experience of being excited about a new QTL repeatedly, and then being disappointed. And lots of personal communication as to the reality of what Carl Shulman is talking about re: publication bias and fiddling around with experiments until the p-value comes out correct from my friends working in genomics, psychology and the interstices.
If I were naked to the field, I would go to google scholar and poke around for the citation history of loci implicated in cognitive performance variation.
"but my impression is that there is a growing list of likely genes"
As I said in my first comment, the list is characterized by non-reproduced associations. I have tracked this sort of research for about 10 years now, and the pattern is a consistent one where a QTL makes a big splash, but there is no follow up. As I also stated, I have friends looking for QTLs which effect normal variation. This is a well known issue in the behavior genetics community.
"My interpretation would be that neither theoretical conssiderations nor empirical studies offer much support to the idea that genes with moderate effects on IQ are particularly uncommon."
Your interpretation is based on unfamiliarity. A literature search would validate that large/moderate QTL effects tend not to be validated over time. In your initial comment you cite ASPM. You obviously don't know the literature, as Rushton looked to see if ASPM variation tracked IQ variation several years ago, and it does not.
Anyway, I guess this is my last comment on this thread. Hope you are more open to being less wrong in the future :-)
Yes, it is very hard. I know, because I know people attempting to find those genes. They report that it's very hard. I specifically said normal variation in IQ to make it clear that I'm not talking about mutations and variants which cause retardation. Those QTLs of large effect are easy to find, but they aren't implicated in normal human variation. How do we know this? Because they don't show up in linkage or association studies consistently.
I didn't say it's impossible. There were many things impossible 10 years ago that are possible now. But I didn't make that assertion in ignorance.
"What about DTNBP1, CHRM2, ASPM, NR2B, HAR1, PYDN?"
Not replicated, or nothing found. ASPM for example isn't associated with normal variation in IQ (or the effect size too small to detect, they've looked). Please see my coblogger "ben g"'s post on the topic:
(and no, I'm not one of the people who is excited that we haven't been able find these genes yet)