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Due to the Ashkenazi "superiority" in terms of IQ when compared to gentile whites, white supremacists would not have struck me too as an obvious first guess.
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:
http://scienceblogs.com/gnxp/2009/01/how_ashkenazi_jewish_are_you.php
In response to
BHTV: Eliezer Yudkowsky & Razib Khan
Down syndrome is not really "on the smallest chromosome". It results from an extra copy of chromosome 21. (22:48).
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.
That truism doesn't sound right to me, but maybe I don't understand it. In the long term, you have equilibrium, but that doesn't mean fixation for genes of small effects, because there are always new mutations. There is an equilibrium between deleterious mutation and selection driving out the mutations; and this is somehow balanced between, say, height and IQ. And none of this is to say there was long-term upward pressure on either trait.
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.
I found Tim's reasoning from published research surprisingly convincing.
Razib "reasoned from published research," too. Rushton doesn't have any PC points to lose. The main heuristic to keep in mind in discussing science is that most published findings are false, especially in popular fields. According to the paper Carl cited, the reported effect sizes are tiny, 0.1 to 1% of variance. The effect sizes are similarly small for genes affecting height; I don't know about replication. In the comments on the gnxp post Razib linked to, Ben G says that if you believed all the reported studies, but corrected for double counting from linkage disequilibrium, the total black-white differential effect is 3 points.
Tim did implicitly cite a replication, in the quote from wikipedia about CHRM2.
Theoretically, it is not so surprising that the effect sizes are small: if there is selective pressure for IQ and height, genes with large effects should be fixed, leaving the variation in genes of small effect.
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).
"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.
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).
Does anyone else here have any familiarity with the field in question? I found Tim's reasoning from published research surprisingly convincing. Yet Razib has given an appeal to his own authority denying that data that also has some credibility behind it.
I don't have the background knowledge to resolve the disagreement myself and I get the impression that the literature will give conflicting viewpoints that are hard for me to unravel in an acceptable amount of time.
My prior p(Tim is right | he is disagreeing with someone else here) isn't very high but my prior p(someone is right | they have made a stand that would be a significantly socially detrimental to change in either the short or long term && their arguing seems oriented to consolidating their own status and questioning the status of the opponent) isn't much different. Actual evidence from Razib would, of course, have dominated other considerations.
I have updated somewhat in the direction of "genes that have some moderate or at least minor but significant correlation with IQ have been identified" but it would be more in my social interest to assert a position of hard agnosticism with respect to IQ-genes for the purpose of affiliation. I am open to persuasion on either the IQ-research evidence or on how my reasoning 'ought-to' go when I encounter this sort of ambiguous input.
I don't think I can trust karma too much in this case as I know my first impulses would bias my voting against Tim and towards the guy blogging heads with Eliezer and so don't expect others to be any different.
"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.
It is hard for me to find an interpretation of "normal variation in IQ" that makes much sense of what you are saying. Also, I note that that phrase was used in an example.
Intelligence has a genetic basis. We know that some things breaking cause large effects - and that other things breaking cause small effects. There will be a bunch of genes that cause effects of intermediate size when they break - and some of those will be broken in relatively normal people - accounting for some of their variation in intelligence.
You could argue that researchers haven't yet found any such genes - but my impression is that there is a growing list of likely genes - from things like the "IQ QTL Project". My interpretation would be that neither theoretical considerations nor empirical studies offer much support to the idea that genes with moderate effects on IQ are particularly uncommon.
No doubt a fair number of such things will actually be caused by genes affecting the gut, muscles, senses, etc - but that gets back to what is meant by a gene "for" intelligence.
"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 :-)
It really isn't hard to find genes for intelligence - assuming that you mean the conventional thing by "a gene for x":
"Maynard Smith reached for a hypothetical example and came up with a 'gene for skill in tying shoelaces'. Pandemonium broke loose at this rampant genetic determinism! The air was thick with the unmistakable sound of worst suspicions being gleefully confirmed. Delightfully sceptical cries drowned the quiet and patient explanation of just what a modest claim is being made whenever one postulates a gene for, say, skill in tying shoelaces.'"
One example:
"Gene found for mental retardation"
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.
In response to
BHTV: Eliezer Yudkowsky & Razib Khan
Not finding genes for IQ? What about DTNBP1, CHRM2, ASPM, NR2B, HAR1, PYDN?
"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:
http://www.gnxp.com/blog/2010/02/half-sigmas-flawed-post-on-dtnbp1.php
(and no, I'm not one of the people who is excited that we haven't been able find these genes yet)
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Got it. Makes more sense with the data. I guess in the flow of conversation, we do tend to miss a couple of things :)
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 :-)