I’ve noticed, over the last year or two, that I’ve stopped reading Slate as much as I used to. I don’t know why, really — I still enjoy some of the pieces I’m occasionally led to on their site. The spirit of Michael Kinsley lives on in some of Jack Shafer’s stuff, and I admit a softness for some of their new Slate V video work. (Their Larry Craig re-enactment was touched by some small amount of brilliance.)
But for some reason I was browsing over there tonight, and I came across this William Saletan piece — “Created Equal” — and I remembered, Ah, this is why.
[Attention Conservation Notice: I’ll be spending the rest of this (longish) post, below the fold, ranting about actually ‘reading’ the articles that you cite in a popular science essay. Read it only if you’re bored, I suppose, and consider this fair warning.]
This is a piece (almost blog-like) that’s part of Saletan’s “Human Nature” series — and he’s writing about “IQ deficits” that split along racial lines. Starting with the condemnation that was heaped on James Watson’s shoulders when he made some pretty egregious comments a little while ago. “Unsupported by science!” shouted pretty-much-everyone, but Saletan sighs heavily, shakes his head more in sadness than in anger, and informs us:
I wish these assurances were true. They aren’t.
Grrrr. Really, I don’t know why I expect better.
For instance, this paragraph caught my eye.
Scientists have already identified genes that influence brain size and vary by continent. Whether these play a role in racial IQ gaps, nobody knows. But we should welcome this research, because any genetic hypothesis about intelligence ought to be clarified and tested.
Ah, really? I didn’t know that.
So I go link-hunting — the first one leads to this paper.
There’s also a second paper in the same issue of Science, by many of the same authors, about a second gene:
Mekel-Bobrov et. al. “Ongoing Adaptive Evolution of ASPM, a Brain Size Determinant in Homo sapiens.”
Seems clear enough, right? There are these gene, MCPH1 and ASPM, that “regulate brain size,” and that show signs of “positive selection.” Case closed?
Well, not quite. Immediately below the original article on the Science web site is a link to this response by Timpson, Heron, Smith, and Enard, “Comment on Papers by Evans et al. and Mekel-Bobrov et al. on Evidence for Positive Selection of MCPH1 and ASPM.” From their abstract,
We genotyped these variants [of MCPH1 and ASPM] in 9000 children and find no meaningful associations with brain size and various cognitive measures, which indicates that contrary to previous speculations, ASPM and MCPH1 have not been selected for brain-related effects.
What’s going on here? It turns out, there’s not actually a strict disagreement between this response and the original paper, according to Mekal-Bobrov and Lahn (two of the original authors) in a response. This is important enough that it’s worth reading a portion of their response in full:
Our greater concern is that Timpson et al.’s comment seems to confuse our report of a genetic signature of selection, which has to do with patterns of genetic variation, with claims regarding specific phenotypic adaptations. Studies of positive selection are rarely based on phenotypic data. Although our ultimate goal is to uncover the phenotype driving the adaptive evolution of a gene, an analysis of genetic variation and divergence is a necessary first step to identify a history of selection. Although a selective event is driven by a phenotypic trait, signatures of adaptation occur at the level of a genotype. This is why a signature of selection is by definition a genetic phenomenon and, by extension, why findings of selection are not in themselves based on phenotype data. Thus, our analyses of positive selection on ASPM and MCPH1 are based entirely on population genetic data and are independent of any claims about the phenotypic effects of these genes. We explicitly stated in our papers that the substrate of selection on these genes might be domains of brain biology other than cognition, or unrelated to the brain all together.
Basically, MCPH1 and ASPM “regulate” brain size. Furthermore, there is independent genetic evidence that these genes are under “positive” selection. But when you look at whether variations of the genes in question actually correlate with differences in brain size and measurements of brain function — no, they don’t. The original authors aren’t fazed by this; it’s entirely possible (likely, even) that the genes regulate other “substrates” of selection as well as something like brain size. “Regulation” is a remarkably malleable word, in genetic terms. But it does undermine Saletan’s implicit claim, since the fact that these genes are under positive selection seems likely to have nothing to do with their regulation of brain function. It’s not that “nobody knows” — we do know, quite a bit.
Look, I’m not trying to argue that there’s no genetic component in the brain stuff that factors into what we commonly call “intelligence.” But his piece is filled with these particularly annoying flourishes that imply that things are scientifically known (or unknown) without actually saying it, that make motions towards explanations while blithely jumping over the details. But if these phenomena are worth understanding, they’re worth understanding in detail. This isn’t useless obscurantism, it’s due diligence.
And my second point is: it took me five minutes — five minutes to track down these links and understand what’s going on here. Apparently that’s five minutes that Saletan didn’t have when he wrote his piece, but this doesn’t augur well for the rest of the ‘facts’ and links that he calmly throws around for the rest of the essay. That he chooses to couch a lot of that language in this kind of pseudo-even-handed “this is creationism for liberals” just makes him come off looking like a cartoon.
I’m obviously not the first, or the smartest, person to point out things like this. Maybe I could go on and on about “unreliable search procedures” in psycho-metric models. Or I suppose I could quote,
Although one would expect most psychologists to subscribe to the thesis that theoretical attributes and measures thereof are distinct — after all, the rejection of operationalism was one of the driving forces behind the cognitive revolution — the standard research procedure in psychology is, ironically, to pretend that it is not true. Both in textbooks on psychological methods and in actual research, the dominant idea is that one has to find an “operationalization” (read: observed score) for a construct, after which one carries out all statistical analyses under the false pretense that this observed score is actually identical to the attribute itself. In this manner, it becomes defensible to construct a test for, say, self-efficacy, sum up the item scores on this test, subsequently submit these scores to analysis of variance and related techniques, and finally interpret the results as if they automatically applied to the attribute of self-efficacy because they apply to the sumscore that was constructed from the item responses.
But maybe the best thing to do is to go back to the guy who probably said it best,
In primitive societies, or so Malinowski taught, myths serve as the legitimating charters of practices and institutions. Just so here: the myth of g legitimates a vast enterprise of intelligence testing and theorizing. There should be no dispute that, when we lack specialized and valid instruments, general IQ tests can be better than nothing. Claims that they are anything more than such stop-gaps — that they are triumphs of psychological science, illuminating the workings of the mind; keys to the fates of individuals and peoples; sources of harsh truths which only a courageous few have the strength to bear; etc., etc., — such claims are at present entirely unjustified, though not, perhaps, unmotivated. They are supported only by the myth, and acceptance of the myth itself rests on what I can only call an astonishing methodological backwardness.
So, you know… what he said.
(And then, what he re-said: the next one’s even funnier.)
[And for that matter, Shalizi links to a paper which deserves a mention of its own: “Brain size does not predict general cognitive ability within families”. It shouldn’t disturb my brother and sister, then, that their heads are not as disproportionate as my own gigantic noggin.]