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.
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.