| | Brad,
"Men have about 6 times the grey matter as women..." Where is all this extra grey matter located? There's not that much extra room inside men's skulls. In women, much of the grey matter is replaced by white matter. Women have at least 6 times as much white matter in their brains as men do (so it is a simple trade-off).
It seemed to me that your view was that I'd have to be superhuman and account for all environmental factors before you'd agree that genetics explains even as much as 0.000001% of the racial IQ gap.
If that is your view, then there's no point in carrying this discussion forward. If it's not, then please explain to me what evidence would move you from thinking racial variation in cognitive capacity likely doesn't exist to thinking it likely does?
Brad, as I said before, I already think that genetics explains somewhere between 15-50% of the observed variation in IQ scores! The reason I think that is because I have produced evidence of environmental factors explaining at least 50% of the observed variation. Now, not everyone knows about the research which I have presented here regarding how environment can and does affect intelligence, so you are still going to get folks -- even intelligence "experts" -- saying that intelligence is primarily genetic. As Robert Atkins the diet guru said, it takes about 20 years before what it is that is scientifically known, becomes scientifically accepted. In his case with low-carb dieting (as well as in the historical examples he gave in his 1972 book) that proved to be true.*
So now, what you would need to show me would be these steps:
1) delineate groupings of genotypes and explain how well of a fit they are (e.g. an 80% fit, a 90% fit) when put into those heuristic categories that we refer to as: "race" 2) show how these groups of genotypes are different from each other in relation to their relative phenotypic expressions of intelligence
The reason you would have to perform step #1 is because the concept of race wasn't deduced from genetic difference, even if genetic differences do, in retrospect, explain the racial variations in phenotypes. The reason you would have to perform step #2 is because of the 'investigative underdetermination ' inherent in such research coupled with genetic/phenotypic redundancy ('genetic overdetermination'). Some "race" could have more of one gene for intelligence, but the other "race" could have more epigenetic factors (or perhaps, say, could have 2 other genes for intelligence -- but genes that are not yet identified) that lead the second race to be the one with more intelligence, on average -- even though all current scientific data would predict that the first one should be more intelligent, on average.
Our investigative underdetermination means that we may not be able to tell which group-activations of which sets of genes produces the phenotypic trait in question (in this case, intelligence) because -- at the same time -- the overdetermination of genotypes means that several combinations of genes, activated in several varieties of activation patterns can (at least, in theory) produce the same phenotypic result (genetic redundancy). An example of genetic redundancy is fetal hemoglobin. We stop producing it as we age and we instead produce adult hemoglobin -- but the genes for fetal hemoglobin never go away, they are still there. They remain there as a possible redundant way to get hemoglobin produced in a person (e.g., to resolve anemia).**
So, you have a set of genes. You have to show that, when activated, they produce intelligence. Also, you have to show that there isn't another set of genes that, when activated, produces the same intelligence. And, even if you successfully show a set of activated genes producing intelligence, you can't be sure that you've shown the only way to produce that phenotypic result from that genotype, because there may be more ways than one combination where the genome could produce the same phenotypic result.
Ed
*Low-carbohydrate diet review: shifting the paradigm.
What does a clinician need to know about low-carbohydrate (LC) diets? This review examines and compares the safety and the effectiveness of a LC approach as an alternative to a low-fat (LF), high-carbohydrate diet, the current standard for weight loss and/or chronic disease prevention. In short-term and long-term comparison studies, ad libitum and isocaloric therapeutic diets with varying degrees of carbohydrate restriction perform as well as or better than comparable LF diets ... . It is time to embrace LC diets as a viable option to aid in reversing diabetes mellitus, risk factors for heart disease, and the epidemic of obesity.
. **Transcriptional regulation of fetal to adult hemoglobin switching: new therapeutic opportunities.
(Edited by Ed Thompson on 1/15, 10:30pm)
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