“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:
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.’”
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.
“There is “a highly significant association” between the CHRM2 gene and intelligence according to a 2006 Dutch family study. The study concluded that there was an association between the CHRM2 gene on chromosome 7 and Performance IQ, as measured by the Wechsler Adult Intelligence Scale-Revised. The Dutch family study used a sample of 667 individuals from 304 families.[59] A similar association was found independently in the Minnesota Twin and Family Study (Comings et al. 2003) and by the Department of Psychiatry at the Washington University.[60]”
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 :-)
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.
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).
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.
Carl’s paper said “most QTL effects may be much smaller than expected—not just 1% effect sizes but perhaps effects as small as .1%”.
That is fine and surely perfectly expected. Most genes have little or nothing to do with intelligence—and so can be expected to have small effects on it.
The paper didn’t say there were no larger effects caused by genetic variation. Genes associated with Fragile X syndrome, Tay-Sachs disease, Neurofibromatosis, etc are known to have larger effects.
Here’s Plomin’s big GWAS largely failing to replicate in 2008. I visited the Russell Sage Foundation last year and talked to the team of IQ Fellows there: James Flynn, Richard Nisbett, and Bill Dickens. I can verify that Razib is just reporting the consensus. And it’s not just a PC consensus: Douglas Knight notes that Rushton agrees with it, as does Arthur Jensen.
“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).
The target seems to have shifted quite a bit since:
“We are not finding any IQ genes”
There are plenty of genes for IQ—if you mean “for” in the standard techincal sense used by geneticists.
The issue has apparently been switched to whether there are any known genes with moderate effect on IQ, once you have ignored all the known genes with huge effects on it. That seems to be a rather more esoteric point—which would apparently need quantifying before being discussed in more detail.
The issue hasn’t been switched, but Razib didn’t (and usually doesn’t) optimize for resistance to misinterpretation in snarky pseudo-correction comments.
Razib and Eliezer were talking about the ability to score embryos based on genomes to select for IQ. To do that, one would need to know alleles responsible for a a substantial fraction of the population variation. Genome-wide-association studies haven’t found those for IQ, where they have for, e.g. skin and eye color. Rare retardation-causing alleles that collectively explain less than 1% of that variation are a sideshow for prediction of population variation, the causes of normal variation differ. So meaningful embryo selection is feasible for skin color, but not for IQ. That’s not esoteric, that was the concrete point in discussion that inspired Razib to mention the state of the search for IQ alleles.
“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)
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”
http://news.bbc.co.uk/1/hi/health/2067864.stm
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.
Here’s an example of the kind of thing I mean:
“There is “a highly significant association” between the CHRM2 gene and intelligence according to a 2006 Dutch family study. The study concluded that there was an association between the CHRM2 gene on chromosome 7 and Performance IQ, as measured by the Wechsler Adult Intelligence Scale-Revised. The Dutch family study used a sample of 667 individuals from 304 families.[59] A similar association was found independently in the Minnesota Twin and Family Study (Comings et al. 2003) and by the Department of Psychiatry at the Washington University.[60]”
http://en.wikipedia.org/wiki/Intelligence_quotient
So: “We are not finding any IQ genes” seems to be rather inaccurate.
I note that there has been at least one negative finding for the same gene:
“No Association Between Cholinergic Muscarinic Receptor 2 (CHRM2) Genetic Variation and Cognitive Abilities in Three Independent Samples.”
http://www.medicine.manchester.ac.uk/research/PubDetails/index.aspx?ID=37741
The study appears to be looking at SNPs—though it tracks quite a number of them. Possibly the relevant variation has a geographic component.
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 :-)
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.
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).
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.
Carl’s paper said “most QTL effects may be much smaller than expected—not just 1% effect sizes but perhaps effects as small as .1%”.
That is fine and surely perfectly expected. Most genes have little or nothing to do with intelligence—and so can be expected to have small effects on it.
The paper didn’t say there were no larger effects caused by genetic variation. Genes associated with Fragile X syndrome, Tay-Sachs disease, Neurofibromatosis, etc are known to have larger effects.
Here’s Plomin’s big GWAS largely failing to replicate in 2008. I visited the Russell Sage Foundation last year and talked to the team of IQ Fellows there: James Flynn, Richard Nisbett, and Bill Dickens. I can verify that Razib is just reporting the consensus. And it’s not just a PC consensus: Douglas Knight notes that Rushton agrees with it, as does Arthur Jensen.
What do you mean when you say ‘not a PC consunsus’? Do you mean “not just what people say because it is the ‘right’ thing to say, it’s actually real”?
Right.
“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).
Thanks Razib, explanation sounds convincing. I think I can take your word on that.
(Also, if your ever find yourself back at LessWrong in the future we use markdown syntax. So ‘>’ gets you a quote.)
A brief overview:
http://en.wikipedia.org/wiki/Heritability_of_IQ#The_search_for_specific_genes
The target seems to have shifted quite a bit since:
“We are not finding any IQ genes”
There are plenty of genes for IQ—if you mean “for” in the standard techincal sense used by geneticists.
The issue has apparently been switched to whether there are any known genes with moderate effect on IQ, once you have ignored all the known genes with huge effects on it. That seems to be a rather more esoteric point—which would apparently need quantifying before being discussed in more detail.
The issue hasn’t been switched, but Razib didn’t (and usually doesn’t) optimize for resistance to misinterpretation in snarky pseudo-correction comments.
Razib and Eliezer were talking about the ability to score embryos based on genomes to select for IQ. To do that, one would need to know alleles responsible for a a substantial fraction of the population variation. Genome-wide-association studies haven’t found those for IQ, where they have for, e.g. skin and eye color. Rare retardation-causing alleles that collectively explain less than 1% of that variation are a sideshow for prediction of population variation, the causes of normal variation differ. So meaningful embryo selection is feasible for skin color, but not for IQ. That’s not esoteric, that was the concrete point in discussion that inspired Razib to mention the state of the search for IQ alleles.
It seems to me as though it is you who is misinterpreting my original question.