Based on not-yet-published 2014 research? I don’t think so.
The whole point is that since we are only at the very precipice of finding these genes, we cannot yet say whether these genes are found with greater frequency in one genetic population or another.
I discussed this and I provided cites to a couple of cluster analyses. And also to Q. Spencer’s discussion. Quote:
Spencer, Q. (2014). The unnatural racial naturalism. Studies in History and Philosophy of Science Part C: Studies in History and Philosophy of Biological and Biomedical Sciences, 46, 38-43.
So, yes it is possible. And yes it did happen. Hence at K=5 with representative sample we get Negroids as a distinct cluster. As for these, see also:
Herráez, D. L., Bauchet, M., Tang, K., Theunert, C., Pugach, I., Li, J., … & Stoneking,
M. (2009). Genetic variation and recent positive selection in worldwide human
populations: evidence from nearly 1 million SNPs. PloS one, 4(11), e7888.
Zhang, Y. (2008). Tree-guided Bayesian inference of population structures.
Bioinformatics, 24(7), 965-971.
I simply can’t believe that anyone would still debate this point.
How border populations fall – e.g., Horn of Africa – is a separate issue form whether deep African populations genetically cluster due to breeding patterns.
LOL. Sure, “negroids” might be a consistent classification if you cut away every population (like these oh-so-inconvenient “border populations”) that blows up that classification. If you want to define this group as “sub-Saharan Africans that don’t include the groups that are closer to non-Africans than to each other”, tautologically, of course, then I suppose it’s consistent. And useless.
Three of the well replicated alleles are from here:
Study published.
A different version of Piffer’s polygenic selection paper was published here:
Piffer, D. (2014). Simple Statistical Tools to Detect Signals of Recent Polygenic Selection. Interdisciplinary Bio Central, 6(1), 1.
The “in press” one repeats the analysis using only well replicated alleles.
If we had 50 alleles we could say. We can’t because we have 4 to 12, depending on standards for inclusion (i.e., how many replications one feels one needs.) My point was that (1) there are (a few) well replicated genes (2) they vary between population (in the predicted manner) (3) this provides (tentative) support/evidence.
Not gonna waste time going over this point by point, which is parsed in such a way that it’s almost unreadable (e.g. references to a nonexistant “1b”, among others). There are a ton of assumptions here that aren’t shared, in addition to referencing uncited research. And all of the things you say we’d “have to dismiss” must be dismissed, because they’re not relevant. Again, if you want to say something about the genes for intelligence in black people, you’ve got to have the genes for intelligence in black people.
I explained the D-race concept.
The smelly old D-racialists happened to point out that races often graduated into one another. And happened to acknowledge that there were hard to assign ethnic groups:
Thus a lack of clear and distinct boundaries and the presence of difficult to assign groups is not a problem for this concept. The point is that (most) Black African populations cluster together on the continental level.
See figure A (near the bottom) here:
Pemberton, T. J., DeGiorgio, M., & Rosenberg, N. A. (2013). Population structure in a comprehensive genomic data set on human microsatellite variation. G3: Genes| Genomes| Genetics, g3-113.
Notice how all of the pretty orange dots (for the map above) (tend to) cluster together?
Yes. A paper published a month ago does show some correlation between these alleles and educational attainment. We’ll see if it stands up to scrutiny over time. But please note that this paper is not identifying genes causally linked to intelligence. As the authors take pains to point out that “the mechanism of their association is unknown” and that they are “possible targets for further studies.”
So while this is an important discovery if it can be repeated, not knowing the mechanism of their function is pretty fatal to supporting your argument in this thread. Without knowing whether and how these genes actually do causally affect educational attainment (much less intelligence), we don’t know whether these genes merely correlate to the myriad social factors responsible for educational attainment. For all we know, these genes are associated with having a face that looks smart, causing people to treat the child as being more smart. Or they correlate to being from an oppressed group, but have no causal relationship to brain function. Or a million other possibilities.
In short, we don’t know if these are brain genes or not. Indeed, the fact that they are much more strongly associated with reading success than with math success would underscore that issue, wouldn’t it?
What do you mean? Where was this established?
I explained why the results of the Scarr study are consistent with a genetic hypothesis. You can read Jensen and Scarr’s back and forth on this in: Scarr, S. (1981). Race, social class, and individual differences in IQ. Psychology Press.
It’s simple math. You start with the question: what magnitude of correlation would a genetic hypothesis predict given the magnitude of genetic differences proposed and the mean and standard deviation of EU ancestry in the AA population? And you go from there.
Also, for the millionth time, specific genes are not needed to determine between group heritability. Read over the discussion here.
Also for the millionth time – if you’re claiming that black people have inferior genes for intelligence, then yes you need the specific genes.
I don’t fundamentally disagree with this. Caution is warranted.
I cited a number of Piffer papers that look at frequency differences using these same alleles and others.
Piffer, D. (2013). Factor Analysis of Population Allele Frequencies as a Simple, Novel Method of Detecting Signals of Recent Polygenic Selection: The Example of Educational Attainment and IQ. Interdisciplinary Bio Central,(1).
Piffer, D. (2014). Estimating strength of polygenic selection with principal components analysis of spatial genetic variation. bioRxiv, 008011.
Piffer, D. (2014). Simple Statistical Tools to Detect Signals of Recent Polygenic Selection. Interdisciplinary Bio Central, 6(1), 1.
(The Ward et al. (2014) paper replicated results from Rietveld et al. (2013); Piffer used Rietveld et al. results. Thus his 2013 paper was able to use alleles replicated again in 2014.)
Forgive me for not reading three more dense academic papers to try to find where they claim that these alleles occur at different rates among D-races. Can you point that out for me?
So you are saying that one can’t use pedigree analysis (e.g., Mendelian genetics) to determine if a trait or trait difference has a genetic basis. This flies in the face of 100 years of behavioral genetic theory. But ok, I have a neat trick. I will define iiandyiiii-genetic evidence as specific alleles based evidence and I will define Chuck-genetic evidence as genetic evidence in the sense including overall genetic similarity and pedigree analysis. I will then contend that:
(1) There is Chuck-genetic evidence for the Race-genetic-intelligence position
(2) Chuck-genetic corresponds better with the historic and contemporary scientific usage of the term. Hence “behavioral genetic” refers to chuck genetic not just iiandyiiii-genetic
e.g.,
See the results section here:
"When considering only the 10 educational attainment alleles, the frequency did not differ between the three races.
In the second ANOVA with 10 educational attainment alleles and the additional 2 IQ increasing alleles, the frequency differed significantly across the three races."
http://www.ibc7.org/data_file/submission/201402/IBC1.000317.01_print.pdf
So, if you want to nitpick, you could say that this paper did not show that IQ-allele freq differed significantly, but only the principle component based on IQ and education alleles. Ok, what whatever. I agree that the results are only tentative. I agree that they constitute iiandyiiii-genetic support, if only very weak.
This should say, “I argue”.
There is nothing in the D-race concept that precludes graduation or " variation based on geographic distance". This graduation was generally acknowledged.
Even in zoology, graduation is not inconsistent with zoological subspecies (formal racial) recognition. Hence:
Population structure refers to the geographic arrangement of local populations across the species’ range. Population structure can be described in terms of three phenomena: the population continuum, geographic isolates, and zones of secondary intergradation (hybrid zones) (e.g., Mayr and Ashlock, 1991). The population continuum is that part of the species’ range where there is continuity of contact among local populations, some of which may be recognized as
subspecies if sufficiently differentiated.
Mascie-Taylor, C. N., Foley, R. A., Jablonski, N., Strier, K., Little, M., & Weiss, K. M. (2003). Gorilla biology: a multidisciplinary perspective. A. B. Taylor, & M. L. Goldsmith (Eds.). Cambridge, UK: Cambridge University Press.
Thus, I don’t see the contrast between race and population continua. It’s a false alternative. (Clines, by the way, are not population continua; they are – or used to be understood to be – character gradients; so there is an important difference between races and clines, at least how clines were traditionally defined. )
The lookism explanation is the most ridiculous ever postulated. Laden is a straight out gene denier.
If you put so much weight on expert opinion why would you dismiss it when it comes to behavioral geneticists’ views about WITHIN group genetic influence – and instead give such weight to “Greg Laden”'s lonesome position.
We see that expert opinion only matters when it supports your position.
Where is your survey on the matter? We discussed a letter – but this only discussed “population genetic” evidence. And no stance was taken regarding all of the evidence. And I explained why the statement was problematic. e.g., they spoke of no pop genetic support for Wade’s speculations but Wade, in fact, never speculated about natural selection for IQ. Refer back to my comments.
For human intelligence? Probably not. Human intelligence is a pretty unique trait.
Silliness not really worth a response.
Let me tackle the three with which you take issue:
If the gaps were the result of nurture, then we would not see them where nurture is reasonably normalized. For example, we would not see huge academic score gaps between children of wealthy and educated black parents and their peers. Those gaps are so enormous that high SES blacks score barely on par with poverty-stricken whites, academically.
We see gene frequency differences for gene variants in all sorts of genes not tied to the ones for self-identification. The medically-oriented genetic literature is full of such examples, as is general physiology. Beyond that, I’ve given you some fairly grand examples; 1-4% (!) of eurasion genomes is considered to be introgressed from archaic Neandertal and/or Denisovan lineages. Those genes are not found in african populations. But basically almost every gene subsequent to the L3/M-N split at out of africa has likely had some changes. We are at the front end in terms of genetic science in finding out how functionally significant those changes are. Sometimes a very minor change (a C for T in HMGA2 may be a candidate example) might drive a significant outcome change. Until those genes are studied, the quantity of changes is unknown, but it is probably much larger than we currently think. In Eric Wang’s study, 1,800 genes were felt to have Darwinian selection in Han, black and european lines. That is, not only did they have significant changes; the changes drove positive selection to the point of significant penetrations. There is absolutely no support for the idea that nature has changed only superficial appearance genes.
All genes are subject to evolution, and therefore post any branching point, descendant lines are way more likely than not to have disparate gene frequencies from lines which descended in parallel but were not subject to admixture.
For example, the MCPH1 haplogroup variant D gene is highly penetrated into eurasian–but not african–lineages; this is thought to be because it arose post L3/M-N split and it may be so highly penetrated because it is an advantageous gene (although I have not seen a study looking at that).
Intelligence is best seen as a trait the outcome for which has a maximal potential determined by genes if nurturing is maximized. That is, we can turn me into a more intelligent person with maximal nurturing, but we can’t turn me into Einstein. Genes do drive intelligence because they are the blueprint for our neurophysiology. Humans are more intelligent than cockroaches, and we don’t need to know which exact genes separate humans and cockroaches to come to a conclusion that a major difference is genes. (I will admit that on occasion my own intelligence has approached that of a cockroach in the opinion of other posters here, but those opinions belong in a different thread. 
) At the same time, “intelligence” is a very loaded term, so I personally think it’s better to talk about a specific skillset, such as a performance on a psychometric exam or an academic test. And there we have very good and broad evidence that existing gaps are never closed even when putative nurturing variables are accounted for such as socioeconomic status or educational opportunity, or both.
It would be nice if we had other measures for neurophysiology which might better quantify functions more likely to have arisen in non-eurasian lines. Surely psychometric tests developed within the paradigm of what one population considers “intelligence” cannot be good measures of neurophysiologic function for other human populations. This is not an argument for cultural variables; we can account for those. It’s an argument that any relatively isolated population is driven by evolution for that discrete environment. Perhaps visual perception is driven over here; motion processing over there; linguistic subtleties in a third population…you get the idea, I hope.
Without the exact genes, you are correct in saying that I make an inference. This is also known as a deduction, and it is based on a stubbornly persistent pattern that is resistant to manipulation and correction for the most obvious nurturing variables. It is also based on the obvious fact that, since all genes are subject to evolution, it is more likely than not that groups separated by historic migration patterns are more likely than not to have disparate gene frequencies.
When we adjust for nurturing, what is left is genes. Were it not for the fact that “intelligence” is a high-value trait, you wouldn’t be “suspecting” an “eagerness” on my part to make this deduction. Indeed, just the opposite is true: the reticence of egalitarians (those who hold on to a hope that nature has created all races approximately egalitarian for traits–and especially high-value traits such as “intelligence” as measured by western proxies for it) to embrace that race-based groupings might have different average neurophysiologic skillsets is a reflection of an eagerness to find equality where none exists anywhere else. Not for appearance; not for physiology; not for gene frequency. Egalitarians are left clinging to the hope that, while all genes have evolved, they have done so without driving any substantive changes for high-value traits.
Hope on.
Perhaps you have some evidence that genes are not at play in driving average outcome differences among races. Would you mind linking some?
I’m not talking about opinions that genes don’t play a role. I just want some frequency studies where it turns out that Gene X, thought to be involved in Functional Outcome Y, turned out to have the same frequency for the same variant of the gene.
An example of the opposite case would be frequency for the carrier state for DARC erythrocyte phenotype Fy(a-b-) by race, and the outcome would be resistance to certain types of malaria…
True. The dispute is over whether they have been reasonably normalized anywhere. I don’t think any non-racist who has given serious study to the history and contemporary effects of racism in the US would contend that the these effects have been reasonably controlled for in any circumstances.
There are some genes that vary in frequency between different self-identified groupings. But that isn’t what you need to show in order to support the inference that if something has a genetic component then it probably differs across self-identified races. To show that, you need to show what I actually said when I stated your premise, which is that “Self-identified race correlates to clusters of genetic similarity/diversity such that we should expect there to be differences in gene frequencies for genes other than those tied up in the self-identification.”
If you take an arbitrary number of groups and a huge number of genes, you are going to find differences in frequencies. But that’s a far cry from the relevant showing.
Yes, obviously. The (sub)question is whether they drive significant differences between humans.