Jerry Fodor, in the _London Review of Books,_ “takes a swing at adaptationism”:http://www.lrb.co.uk/v29/n20/fodo01_.html in the name of Evo-Devo. I’m not sure that he lands any really new or heavy blows, but I have only read it once and I am more than usually stupid with a cold this morning. Germane, perhaps, is a letter from a friend in Boston:
bq. Teaching my evolutionary biology course again this fall – I’ve re-read the Sean Rice textbook now for the 4th time, and it’s really on the money. One can *prove* — prove in the sense of proof – that there’s exactly *one* modeling case where the Dawkins’ gene’s-eye-view *makes the right predictions* – which
is all a scientist cares about – and in *all the other cases* – ie, 99.99% of biology – it doesn’t work … In the sense of: it gives the WRONG predictions.
Thus it is not a matter of semantics or armchair philosophy about ‘levels of selection’ — it is simply like getting the thing wrong, like saying there are ‘clumps’ like OH instead of molecules or atoms.
It’s just that way. Tough luck. But that’s really how it is. In every other case – if there’s sex, fertility selection, if selective forces change with varying allele frequency (density dependence); if an individual’s striving for increased fitness reduces the mean population fitness — all of these situations illustrate the failure of the Dawkins view.
Yet, this goes unsaid. It also indicates that evolutionary psychology, as I understand it cannot possibly succeed if it takes ‘allele frequency’ as its central driving principle.
Doesn’t this mean that Dawkins is yer actual bollocks?
Sounds like a story to me! (OK, more dog bites man, but still – there’s a lot of people saying that this particular dog is nothing of the sort)
The difficulty with the claim that “Dawkins is bollocks” is that he contradicts himself so much that he has to be right. The big rhetoric is always picked apart in the small print; and his definition of “gene” is far more elastic than a mere allele.
But, of course, a shifting of allele frequencies is a shift in counters for something. It seems to me that the fundamental problem is that the gene’s-eye-view gets the arrow of causation the wrong way round. We know that changing selective pressures will change allelic frequencies. You can’t go the other way, though, and assume that a change in allelic frequencies tracks a change in selective pressure. You might in some cases show that it does, though the complications mentioned by my correspondent make this mathematically difficult. You can hypothesise that a particular change does track a particular selective pressure and see where that gets you. But it may not get you very far.
The hot question this week is whether there are genes for promiscuity — see DSW note above. But I am not goig to do it until I have finished some other stuff.
I don’t know about genes for promiscuity, but isn’t there a correlation between certain aspects of primate genital anatomy and their bearers’ shagging habits? Or are you talking about variations within a single species (presumably, us), where I don’t believe any rigorous studies have been done (self-selecting samples, as viewable on the Internet, notwithstanding)?
Rupert, the genes for promiscuity thing was about variation among humans, not the testicle size comparisons which are used to make estimates of monogamy among different species. But, as I say, it needs research.