[ QUOTE ]
Edited for link:
http://www.halfsigma.com/2007/10/race-difference.html
[/ QUOTE ]
To follow up on this link that was posted, the title of which is, "Race difference in intelligence: does genetic proof already exist?", I asked someone knowledgeable on the subject about it. Not surprisingly, it's discussion of "high intelligence genes" and how they can even now be applied to "race" is completely fallacious, and this link here does a terrific job explaining why:
Brain Evolution, Population Genetics and Armchair Kookery
Although this blog (being from 2005) was not written specifically in response to the quoted link, it might as well have been. For those not inclined to follow the link, I'll post a section of the text here:
<font color="brown">
"Before getting down to business, I'd like to start off with a brief discussion on some rudiments of population genetics and how it relates to the work done by actual biologists who spend their time sussing out the often extremely convoluted details of how genes are translated into all those proteins which govern how organisms function. A common misconception many people have of how things work is that there are one or a few genes "for" this trait or that one, the presence of absence of which determines whether an organism will or will not manifest a particular trait; a related misconception is that a gene which influences one particular trait will have an effect on that trait only or even primarily, and that therefore any allelic differences we notice must pertain to whatever phenotypical differences we think we already know they're responsible for. If both of these things were true, population genetics would be a much more tractable subject, but unfortunately, neither is even close to accurately describing reality.
The truth about the way genes work is that other than in the case of simple mendelian traits of the kind which geneticists have had most success studying during the last century, it is almost unheard of in genetics research to discover single genes which are able to account for more than a minute fraction of variation in any given trait; furthermore, the very reason why so many traits in any given population happen to abide by a normal distribution is because to the extent said traits aren't determined by environmental differences, they must be under the influence of very many genes, and the smoother the curve, the greater the number of underlying genes must be - this is nothing more than a generalization of the binomial theorem with which we are all familiar. In the case of the human brain, we know that about half of all genes - or some 15,000 of the total - are expressed in the brain during the course of development, and there is no a priori reason to believe that variations in any of them, or even in whatever regulatory regions might govern their behavior, will have no impact on how said organ functions. In light of all the foregoing, anybody who thinks we will find 20 or even 50 genes which rigorously account for, say, 90% of all "genetic" variation in "IQ" or whatever nebulous measure of intellect we decide upon is a fool at best.
Having discussed the "one trait -> one or a few genes" fallacy, let me turn now to its counterpart, namely the belief that a gene's only or main function must be to determine any single particular trait (hence all the idiotic talk of genes "for" IQ, homosexuality, jazz improvisation, etc.). Genes code for proteins, not explicit traits, and it is part of the blind genius of evolution that individual proteins are co-opted to serve multiple roles all the time, so much so that there is even a technical name for the phenomenon, to whit, pleiotropy. Underlying all the ignorant chatter about how the ASPM and microcephalin variants written about by Dr. Lahn must be genes "for" cognition is the assumption that because faults in both genes have been implicated in brain disorders, and because differences exist between humans and chimps in both genes, then "the" purpose of the existence of these new variants has to be to code for "IQ" or some such thing: but the reality is that with an organ as complex as the human brain, there are very many ways for a gene malfunction to lead to devastating consequences, often through causal chains nobody would have guessed beforehand.
To illustrate how things aren't always what they seem, and why it is important to understand the underlying biochemistry before jumping to conclusions, let us consider phenylketonuria: this is a genetic disorder which is characterised by mental retardation, and an uninformed observer might easily jump to the conclusion that this means defects in the gene implicated in it must result in some crucial feature of the brain being wired wrongly, leading to lower IQ scores. And yet, as we now know, the depressed IQ which accompanies phenylketonuria has nothing to do with brain wiring, but is the result of an inability of the sufferers' metabolic systems to produce sufficient levels of phenylalanine hydroxylase: in the presence of a diet which makes up for this deficiency, the IQ scores of the genes carriers turn out to be normal, and what might have been ascribed to an "IQ gene" is in fact just one particularly visible manifestation of an enzyme deficiency which has several other side-effects.
The misconceptions about how genes work extend beyond these two errors, however, and there's a third issue I'd like to discuss which goes by the technical name epistasis. The basic idea behind this term is that if genes at more than one locus govern the expression of a trait, they need not do so in a straightforward, additive fashion like so many dollars which can be netted against each other - even if a gene happens to code for a particular phenotype, it could well be that the trait will not be expressed in the slightest if the allele at some other gene locus isn't the right one. To give an example, suppose there are two genes which govern hair color in mice, with gene A coding for an enzyme which produces the melanin which makes hair black, and gene B coding for another enzyme which modifies the product of gene A so that the resulting hairs are grey (agouti): if a mouse happens to be carrying two broken copies of A, then that mouse is destined to an albino, regardless of how well its copies of B might function, as the enzymes which the products of B alter simply won't be produced. The point here is that an error or variation at some step in a multistep biochemical pathway can suffice to alter the rest of the successive steps in such a way that simplistic totalling of the presence or absence of alleles "for" this or that leads to completely wrong results: genetic background matters, and even if a gene can be shown to affect the expression of a trait in a particular population, there's no reason to believe it will also do so in a different population, even if we are able to adequately control environmental variation (this isn't merely theoretical - see, for instance, this paper, which finds that APoE, although repeatedly implicated as a risk factor for Alzheimer's disease amongst white Americans, is not associated with elevated risk in either African-Americans or Hispanics)." </font>
The rest of the blog is well worth reading, see the link.