# At what level is racialism accepted in the scientific community? **URL:** \ **Category:** Great Debates\ **Created:** [August 10, 2014, 6:55pm UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257 "2014-08-10T18:55:39Z")\ **Posts on this page:** 20\ **Page:** 11
**Author:** ![GIGObuster](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/gigobuster/32/421_2.png) [@GIGObuster](https://boards.straightdope.com/u/GIGObuster)\ **Post date:** [August 18, 2014, 3:50pm UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/201 "2014-08-18T15:50:03Z")
> [@Chuck11](#): > > What counts as “genetic evidence”. These are the types of genetically informed lines of evidence available: Not a pertinent cite about genetics or the mechanics of the genes that they usually do not point or identify. > [@Chuck11](#): > > The survey results were only recently presented in a 2014 conference on intelligence. How could it have been pointed at for years? This is why you are really the one that has not paid attention. The makers of the surveys are an old darling of the pseudoscience racists. As the cite you made points out: “So, when finding out about real opinions, anonymity is required. Rindermann, Coyle and Becker have replicated the last survey on experts done 30 years ago” And your group before used a similar ruse: [http://boards.straightdope.com/sdmb/showpost.php?p=13693853&postcount=501](http://boards.straightdope.com/sdmb/showpost.php?p=13693853&postcount=501) As I said that is just horse puckey, the survey did not include anthropologists or biologists, and few geneticists. Whoever did those surveys are playing loose and fast with what an expert in the matter is, as it was in reality a grab bag of diverse fields that they surveyed. This is using a similar tactic as the survey the global warming deniers did showing that 32000 experts do not see that humans are causing the current warming that is being observed: > **[32000 Scientists](https://thinc.blog/2010/01/09/32000-scientists/)** > > 32,000 leading scientists signed a petition against global warming? Is that really true?  Well, no… But to get to the bottom of this crock, we’ll have to go back in history, and meet so… The tactic is to avoid surveying the experts that count so as to get the results the pseudo scientists want. Same old same old. Again, the issues remain, a very low reply rate, and the people consulted are indeed not looking at the whole of the evidence, as pointed by other examples like the other survey from meteorologists that pondered about climate science those levels of misunderstanding of what other more pertinent experts conclude is not extraordinary. Plain ignorance explains it, your claim about them looking at the totality of the science is silly since there is no science linked at in the survey you pointed out, what remains just the opinion of intelligence experts that should know better. ---
**Author:** ![Evil\_Economist](https://avatars.discourse-cdn.com/v4/letter/e/c89c15/32.png) [@Evil\_Economist](https://boards.straightdope.com/u/Evil_Economist)\ **Post date:** [August 18, 2014, 4:05pm UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/202 "2014-08-18T16:05:41Z")
> [@Chuck11](#): > > (Edits. Sorry, it’s late. I’ll continue another time.) > > I said “self reported ancestry”. I did some analyses myself – though I haven’t got around to publishing (in an open psych journal, of course). The primary sources (e.g., Add Health, NLSY79, NLSY97) are publicly accessible so you can verify if you want. > > [More than Just “Colorism”: Part 1. – Human Varieties](http://humanvarieties.org/2013/02/02/more-than-just-colorism-part-1/) > > [Self-reported white ancestry among US blacks : A Jensen effect – Human Varieties](http://humanvarieties.org/2013/04/27/self-reported-white-ancestry-among-us-blacks-a-jensen-effect/) > > [Skin Color is Not Driving the Relationship Between Racial Admixture and IQ – Human Varieties](http://humanvarieties.org/2013/02/09/skin-color-is-not-driving-the-relationship-between-racial-admixture-and-iq/) > > I guess – except that IRBs won’t grant approval, so the type of data isn’t available. Of course, a hereditarian could collect data on their own. I think that’s where the intellectual laziness comes in. For example, one could use SAT scores and 23andME admixture results. The thing is it would be hard to get critics to believe. When you use national data, on the other hand, the raw data isn’t suspect. I’m also interested in this. When you say “self-identified African Americans with higher levels of European ancestry score higher on IQ tests,” I expect peer-reviewed published journal articles showing this. I read one of your “cites” and it not only wasn’t it a published journal article, it would never be accepted as a journal article because of the glaring errors that were immediately evident on even a cursory examination. ---
**Author:** ![Belowjob2.0](https://avatars.discourse-cdn.com/v4/letter/b/b9e5f3/32.png) [@Belowjob2.0](https://boards.straightdope.com/u/Belowjob2.0)\ **Post date:** [August 18, 2014, 6:34pm UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/203 "2014-08-18T18:34:21Z")
> [@Richard\_Parker](#): > > I have a question for those who know more about genetics. How does epigenetics play into all of this? My impression is that we are in the early stages of understanding epigenetic phenomena, but that we believe at least some of the differences in inherited traits is due not to different genes but to different experiences of recent ancestors. So, for example, if someone’s grandparent experienced a famine they may process insulin differently–not because they have different genes, but because the actual mechanism of expression is changed epigenetically. > > If all of that is correct, it seems like an error to conflate heritability and genes. Even if a trait is shown to be heritable, the cause could be epigenetic rather than genetic. Doesn’t it seem entirely plausible that brutally oppressing a population of people will cause several generations of their descendants to express genes (the same genes everyone else has) in different ways, if the epigenetic hypothesis is true? There’s ongoing inquiry into this phenomenon: > **[Epigenetics and IQ variability](https://forwhattheywereweare.wordpress.com/2012/10/18/epigenetics-and-iq-variability/)** > > A new study on monozygotic (identical) twins with clear IQ differences finds that epigenetic methylation of certain genes may be the cause: Chih-Chieh Yu, Genome-Wide DNA Methylation and Gene Expre… > **[Genome-Wide DNA Methylation and Gene Expression Analyses of Monozygotic Twins...](https://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0047081)** > > Human intelligence, as measured by intelligence quotient (IQ) tests, demonstrates one of the highest heritabilities among human quantitative traits. Nevertheless, studies to identify quantitative trait loci responsible for intelligence face... > [@](#): > > Epigenetics and IQ variability > > 18 > OCT > A new study on monozygotic (identical) twins with clear IQ differences finds that epigenetic methylation of certain genes may be the cause: > Chih-Chieh Yu, Genome-Wide DNA Methylation and Gene Expression Analyses of Monozygotic Twins Discordant for Intelligence Levels. PLoS ONE, 2012. Open access ··\> LINK [doi:10.1371/journal.pone.0047081] > Abstract [http://coglab.wjh.harvard.edu/~cfc/Chabris2012a-FalsePositivesGenesIQ.pdf](http://coglab.wjh.harvard.edu/~cfc/Chabris2012a-FalsePositivesGenesIQ.pdf) > [@](#): > > Most Reported Genetic Associations > With General Intelligence Are Probably > False Positives > [@](#): > > What our results show is that the way researchers have been looking for genes that may be related to intelligence — the candidate gene method — is fairly likely to result in false positives, so other methods should be used. The speculation being that the false positives were caused by environmental effects, particularly epigenetic changes. ---
**Author:** ![Richard\_Parker](https://avatars.discourse-cdn.com/v4/letter/r/35a633/32.png) [@Richard\_Parker](https://boards.straightdope.com/u/Richard_Parker)\ **Post date:** [August 18, 2014, 7:47pm UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/204 "2014-08-18T19:47:09Z")
> [@Fotheringay-Phipps](#): > > The related question is: where does this hypothesis fall in terms of the “racist scum” scale? > > Because suppose you bought into this, you would be then saying that the genetic differences are not inherent to the group, in the sense that it could change back relatively quickly in future generations (as compared to evolution), but would still be saying that the genetic differences are inherent to the current members of the group. > > Is that acceptable from a PC standpoint? AFAICT, the racist scum assessment comes from a few moves made by the “racialists”: (1) Defense of the arbitrary separation of people into traditional racial categories instead of more coherent populations. There is no good defense for using Caucasians, Asians, and Africans as genetic populations. (2) Using weak circumstantial inferences to reach traditional racist conclusions, when if anything the burden on people reaching those conclusions should be heightened rather than lowered. (3) Denial of the history of white supremacy in the United States as way to minimize the likelihood that so-called “nurture” factors explain outcome disparities here. I don’t think anyone is saying that it is inherently un-P.C. to scientifically conclude that a gene linked to intelligence is less prevalent in a given population. Instead, the objection is that this isn’t what the racialists are doing in any coherent way, and appear instead to be doing pseudoscience to serve racist agenda. At most, (2) could be applied to this epigenetic hypothesis, but I think no one is arguing that we really know anything about how epigenetics works. The notion is more that the hypothetical possibility of this epigenetic mechanism casts even further doubt on notion that we can pretty well guess–based on current evidence–that intelligence is going be the subject of genes with different frequencies across large populations. ---
**Author:** ![Chief\_Pedant](https://avatars.discourse-cdn.com/v4/letter/c/a6a055/32.png) [@Chief\_Pedant](https://boards.straightdope.com/u/Chief_Pedant)\ **Post date:** [August 18, 2014, 7:58pm UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/205 "2014-08-18T19:58:19Z")
> [@Belowjob2.0](#): > > There’s ongoing inquiry into this phenomenon: > > [Epigenetics and IQ variability | For what they were... we are](http://forwhattheywereweare.wordpress.com/2012/10/18/epigenetics-and-iq-variability/) > > [Genome-Wide DNA Methylation and Gene Expression Analyses of Monozygotic Twins Discordant for Intelligence Levels](http://www.plosone.org/article/info:doi/10.1371/journal.pone.0047081) > [http://coglab.wjh.harvard.edu/~cfc/Chabris2012a-FalsePositivesGenesIQ.pdf](http://coglab.wjh.harvard.edu/~cfc/Chabris2012a-FalsePositivesGenesIQ.pdf) > > The speculation being that the false positives were caused by environmental effects, particularly epigenetic changes. Epigenetics to explain variations between monozygotic twins, maybe, where the DNA gene pools are so similar. It’s not a reasonable explanation at large scale for populations unless you have some credible driver for it. Your third cite (bottom of P7) suggests the problem is that a given variant may have only a tiny effect, and therefore very large scale studies are needed for each candidate gene to get rid of false positives. ---
**Author:** ![Chuck11](https://avatars.discourse-cdn.com/v4/letter/c/96bed5/32.png) [@Chuck11](https://boards.straightdope.com/u/Chuck11)\ **Post date:** [August 19, 2014, 4:01am UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/206 "2014-08-19T04:01:13Z")
> [@Richard\_Parker](#): > > I have a question for those who know more about genetics. How does epigenetics play into all of this? My impression is that we are in the early stages of understanding epigenetic phenomena, but that we believe at least some of the differences in inherited traits is due not to different genes but to different experiences of recent ancestors. So, for example, if someone’s grandparent experienced a famine they may process insulin differently–not because they have different genes, but because the actual mechanism of expression is changed epigenetically. > > If all of that is correct, it seems like an error to conflate heritability and genes. Even if a trait is shown to be heritable, the cause could be epigenetic rather than genetic. Doesn’t it seem entirely plausible that brutally oppressing a population of people will cause several generations of their descendants to express genes (the same genes everyone else has) in different ways, if the epigenetic hypothesis is true? Interestingly, pre-Darwinian racial theories (e.g., those of Buffon) were often proto-epigenetic. Whatever the case, epigenetics can’t account for much cognitive ability variance within populations, so it’s very unlikely that it account for much between. Just do the math. A simplified model: total variance = additive genetic + non additive genetic + shared environmental + unshared environment and error + epigenetic + other e…g, G x E total variance = 100 additive genetic = lower bounds = 40 to 50 (age depending) as estimated by GCTA additive variance not captured by common variants (and not picked up by GTCA) = ? non additive genetic = at least 10 (age depending) (epigenetics wouldn’t, from what I have been told, mimic this) shared environmental = 20 to 10 (some say zero by adulthood, but I can’t believe this) (age depending) based on Adopted sib correlations unshared environmental + error = 20 based on twin/sibling discordance Epigenetics = ? Other = ? There just isn’t much room for epigenetic influence. In the pre-GCTA era this would have made a good argument. But GCTA establishes a _substantial lower bounds narrow_ heritability, so there is little explanatory room for epigenetics – at least for IQ. ---
**Author:** ![Richard\_Parker](https://avatars.discourse-cdn.com/v4/letter/r/35a633/32.png) [@Richard\_Parker](https://boards.straightdope.com/u/Richard_Parker)\ **Post date:** [August 19, 2014, 1:29pm UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/207 "2014-08-19T13:29:12Z")
I don’t know anything about GCTA software, but I’m skeptical of your claims that it establishes hard boundaries for variance caused by different variables. My feeble googling suggests that it is good at estimating the variance associated with different sequence variations. How does it set the lower bounds for genetic heritability? ---
**Author:** ![Fotheringay-Phipps](https://avatars.discourse-cdn.com/v4/letter/f/d9b06d/32.png) [@Fotheringay-Phipps](https://boards.straightdope.com/u/Fotheringay-Phipps)\ **Post date:** [August 19, 2014, 4:11pm UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/208 "2014-08-19T16:11:49Z")
> [@Richard\_Parker](#): > > AFAICT, the racist scum assessment comes from a few moves made by the “racialists”: > > (1) Defense of the arbitrary separation of people into traditional racial categories instead of more coherent populations. There is no good defense for using Caucasians, Asians, and Africans as genetic populations. > > (2) Using weak circumstantial inferences to reach traditional racist conclusions, when if anything the burden on people reaching those conclusions should be heightened rather than lowered. > > (3) Denial of the history of white supremacy in the United States as way to minimize the likelihood that so-called “nurture” factors explain outcome disparities here. > > I don’t think anyone is saying that it is inherently un-P.C. to scientifically conclude that a gene linked to intelligence is less prevalent in a given population. Instead, the objection is that this isn’t what the racialists are doing in any coherent way, and appear instead to be doing pseudoscience to serve racist agenda. > > At most, (2) could be applied to this epigenetic hypothesis, but I think no one is arguing that we really know anything about how epigenetics works. The notion is more that the hypothetical possibility of this epigenetic mechanism casts even further doubt on notion that we can pretty well guess–based on current evidence–that intelligence is going be the subject of genes with different frequencies across large populations. The thing is that a lot of the “racist scum” are not doing any of the things that you list (and there are other factors as well, FWIW), but are simply being lumped in and associated with the others who are. So the question still remains as to whether epigenetics proponents would be treated similarly. [Personally I suspect that what might tip the scales is the epigenetics proponents emphasizing it being the result of persecution etc., which would cover them somewhat.] ---
**Author:** ![Grim\_Render](https://avatars.discourse-cdn.com/v4/letter/g/a87d85/32.png) [@Grim\_Render](https://boards.straightdope.com/u/Grim_Render)\ **Post date:** [August 19, 2014, 5:46pm UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/209 "2014-08-19T17:46:32Z")
You know, my first degree was Biochemical Engineering. That was over 20 years ago, of course, and I only worked in the area for a year afterwards. The field has changed a lot in the time since. However, I’ve tried to keep up with population genetics form an interest in the subject. So here is my semi-educated opinion on the matter: > [@orcenio](#): > > In April 28th of this year, Nicholas Wade authored a book called “A Troublesome Inheritance: Genes, Race, and Human History” I read a free copy of the book (it’s quite a short and easy read) and I’d summarize it in a few points: > > 1. Humans are biologically clustered into the “5 major races.” > [@furt](#): > > Having recently read the book, IMO, this is an inaccurate and unfair summary. > > The book is divided into 2 parts. > > The first is an attempt to survey the recent findings of the relevant sciences, Mainly, he contends: > 2) That there are distinct population clusters that generally correspond to the traditional Caucasion/African/Asian/Aboriginal racial identifications. This is the point where I would just put the book down and move on. To the best of my knowledge, this is not just wrong, but frothingly wrong. Most genetic variety are found in Africa. The greatest genetic outlier among populations is the Khoe-San people. They diverge far more from the rest of humanity than for example Africans and Eskimos do. Or any other two population groups. In fact the genetic divergence between the Khoe and San subgroups is comparable to the difference between Europeans and American Indians. Then there is Africa. The gentic diversity in Africa is bigger than the rest of the worlds total diversity. It is like someone wanted to compare genetic variations in dog breeds and decided that a reasonable way to group dog genetic diversity was “_Irish Setter_” - “_English Setter_” - “_Gordon Setter_” - “_Irish Red and White Setter_” - and “_Every other dog plus wolves_” It is immediatly obvious that these are not fuctional groups of dog genetic diversity. If you were to make honest groups of human population based on genetic variety to call “Race”, you’d end up with most of them being African groups. Wades “race” groups is not based on scientific knowledge. They are instead based on the “race” concept of 18th century supremacists and Aryan power groups. Thats the point at which I’d leave the book behind as a waste of time. On the raised subject of comparisons between African Americans and caucasians, remember that people exchange genes all the time, and most genes don’t cluster. Slavery ended 150 years ago, at which point african immigration to the US will have declined severely. American blacks are a group defined by the presence of a number of the genes that determine skin color. Whether any other genes have flollwed these genes down the generations is hard to say. On eipgenetics, remember that the signal from epigenetics will not be the same in an individual as in a population. The Duch famine of 1944, as I remmeber, is where epigenetic effects were first noticed. The signal, in this case reduced height, is not neccessarily noticable in an individual, but will be exceptionally clear over a population. ---
**Author:** ![Chuck11](https://avatars.discourse-cdn.com/v4/letter/c/96bed5/32.png) [@Chuck11](https://boards.straightdope.com/u/Chuck11)\ **Post date:** [August 19, 2014, 7:34pm UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/210 "2014-08-19T19:34:58Z")
> [@Richard\_Parker](#): > > I don’t know anything about GCTA software, but I’m skeptical of your claims that it establishes hard boundaries for variance caused by different variables. My feeble googling suggests that it is good at estimating the variance associated with different sequence variations. How does it set the lower bounds for genetic heritability? The authors discuss the method here: Yang, J., Lee, S. H., Goddard, M. E., & Visscher, P. M. (2011). GCTA: a tool for genome-wide complex trait analysis. The American Journal of Human Genetics, 88(1), 76-82; Yang, J., Manolio, T. A., Pasquale, L. R., Boerwinkle, E., Caporaso, N., Cunningham, J. M., … & Visscher, P. M. (2011). Genome partitioning of genetic variation for complex traits using common SNPs. Nature genetics, 43(6), 519-525. Here’s a pity discussion: “In GCTA, researchers use DNA data for hundreds of thousands of SNPs from unrelated individuals to estimate genetic influence on a particular trait. Unlike the hypothesis-testing approach of GWAS, GCTA does not specify which DNA variants are associated with a measured trait. Instead, it is a parameter-estimation approach that relates similarity in SNPs to phenotypic similarity between pairs of individuals. The use of a large sample, together with pair-by-pair comparisons, allows amplification of the weak signal derived from the low genetic similarity between unrelated subjects. Heritability is estimated as the extent to which genetic similarity can account for phenotypic similarity. (Plomin, R. (2012). Genetics: How intelligence changes with age.)” The principle is the same as that with kinship studies, you are just indexing genetic similarity with SNPs. This allows you to look at the genetic/phenotypic correlation among random individuals, thus removing the confounds of epigenetics and shared environments. ---
**Author:** ![Chuck11](https://avatars.discourse-cdn.com/v4/letter/c/96bed5/32.png) [@Chuck11](https://boards.straightdope.com/u/Chuck11)\ **Post date:** [August 19, 2014, 7:54pm UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/211 "2014-08-19T19:54:37Z")
> [@Grim\_Render](#): > > If you were to make honest groups of human population based on genetic variety to call “Race”, you’d end up with most of them being African groups. Wades “race” groups is not based on scientific knowledge. They are instead based on the “race” concept of 18th century supremacists and Aryan power groups. Black African populations cluster together, meaning that a random Black African will be more genetically similar to another than to a non-Black African when a large number of alleles are looked at, because there were less barriers to interbreeding within Africa than between Africa and out-of-Africa. [http://www.sciencedirect.com/science/article/pii/S0002929710003642](http://www.sciencedirect.com/science/article/pii/S0002929710003642) On the other hand, there is higher than average genetic diversity because you began with more diverse populations to start. > [@](#): > > On the raised subject of comparisons between African Americans and caucasians, remember that people exchange genes all the time, and most genes don’t cluster. Slavery ended 150 years ago, at which point african immigration to the US will have declined severely. American blacks are a group defined by the presence of a number of the genes that determine skin color. Whether any other genes have flollwed these genes down the generations is hard to say. Ridiculous. We have a pretty good idea about [how West African African Americans are.](http://www.biomedcentral.com/content/pdf/gb-2009-10-12-r141.pdf) > [@](#): > > On eipgenetics, remember that the signal from epigenetics will not be the same in an individual as in a population. The Duch famine of 1944, as I remmeber, is where epigenetic effects were first noticed. The signal, in this case reduced height, is not neccessarily noticable in an individual, but will be exceptionally clear over a population. If epigenics counts for very little variance within groups, then it’s unlikely to count for much between groups. It could, of course, as could some magical x-factor that only works between populations. But it’s unlikely and would be very difficult if impossible to empirically evaluate. ---
**Author:** ![Richard\_Parker](https://avatars.discourse-cdn.com/v4/letter/r/35a633/32.png) [@Richard\_Parker](https://boards.straightdope.com/u/Richard_Parker)\ **Post date:** [August 19, 2014, 8:06pm UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/212 "2014-08-19T20:06:13Z")
> [@Chuck11](#): > > Here’s a pity discussion: “In GCTA, researchers use DNA data for hundreds of thousands of SNPs from unrelated individuals to estimate genetic influence on a particular trait. Unlike the hypothesis-testing approach of GWAS, GCTA does not specify which DNA variants are associated with a measured trait. Instead, it is a parameter-estimation approach that relates similarity in SNPs to phenotypic similarity between pairs of individuals. The use of a large sample, together with pair-by-pair comparisons, allows amplification of the weak signal derived from the low genetic similarity between unrelated subjects. Heritability is estimated as the extent to which genetic similarity can account for phenotypic similarity. (Plomin, R. (2012). Genetics: How intelligence changes with age.)” > > The principle is the same as that with kinship studies, you are just indexing genetic similarity with SNPs. This allows you to look at the genetic/phenotypic correlation among random individuals, thus removing the confounds of epigenetics and shared environments. Let’s see if I understand. So the software looks at a whole bunch of SNPs (not targeting any particular genes necessarily), and then comes up with some assessment of genetic similarity between two individuals based on similarity of SNPs. The more variation in the sampled SNPs, the more the two individuals can be assumed to be genetically distant. It then looks to some kind of phenotypic similarity–say, thigh circumference–and estimates the extent to which genetic similarity accounts for the phenotypic similarity. I assume it does some fancy math here to compare how well the genetic variation tracks the phenotypic variation. Is that it, or is there something more to it? Because if that’s it, I don’t think it does what you’re claiming. ---
**Author:** ![Chuck11](https://avatars.discourse-cdn.com/v4/letter/c/96bed5/32.png) [@Chuck11](https://boards.straightdope.com/u/Chuck11)\ **Post date:** [August 19, 2014, 9:33pm UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/213 "2014-08-19T21:33:55Z")
> [@Richard\_Parker](#): > > AFAICT, the racist scum assessment comes from a few moves made by the “racialists”: > > (1) Defense of the arbitrary separation of people into traditional racial categories instead of more coherent populations. There is no good defense for using Caucasians, Asians, and Africans as genetic populations. When you take representative samples – i.e., don’t over-flavor with certain ethnic population – you get results like figure 7 here: Jombart, T., Devillard, S., & Balloux, F. (2010). Discriminant analysis of principal components: a new method for the analysis of genetically structured populations. BMC genetics, 11(1), 94. Generally, black African groups cluster together because there was lots of boom-boom in Africa. Of course, if you load the sample with Black African, etc populations this will distort the results. The African American philosopher Q. Spencer explained this point: > [@](#): > > First, some levels of genetic clustering corresponded nicely with certain folk racial classifications. For example, at K = 3, the clusters picked out Mongloids, Caucasoids, and Negroids. Furthermore, at K = 5, the clusters picked out current U.S. Census races: Sub-Saharan Africans (hereafter ‘‘Black Africans’’), Caucasians, East Asians, Amerindians, and Oceanians. K = 6 was similar to K = 5, except it had a single Pakistani population (the Kalash) in a part all by itself. A second interesting result was that the level of populations with the highest among-part genetic variance (r2a ) was K = 5, which was 4.3 ± 0.40 at 95% confidence (Rosenberg et al., 2002, p. 2382). This last result seemed to support Risch et al.’s famous claim that ‘‘genetic differentiation is greatest when defined on a continental basis’’ (Risch, Burchard, Ziv, & Tang, 2002, p. 3). Despite these promising results for racial naturalism, Hochman argues that the genetic clusters of human populations identified in Rosenberg et al. (2002, 2005), and in other similar genetic studies, do not satisfy any of (a)–(d). > > First, citing Ning Yu, Chen, Ota, and Li (2002), Hochman (2013, pp. 336, 349) points out that Black Africans house the most genetic diversity out of any ‘‘continental population’’. In fact, according to Yu et al. (2002), Black African subpopulations are more genetically different than Black Africans and Eurasians. Specifically, Yu et al. (2002, p. 269) found that the average nucleotide diversity (p) for 50 autosomal noncoding DNA segments (with 146 single nucleotide > polymorphisms, or ‘‘SNPs’’) in 10 Black Africans (from 9 populations) was 0.115 ± 0.016%, while p for the same DNA segments and SNPs between the same sample of Black Africans and 20 Eurasians (from 20 populations) was only 0.096 ± 0.012%. The calculations were repeated using other autosomal and X-linked regions (Yu et al., 2002, p. 273). The result appeared to be robust that > there is more genetic diversity in Black Africans than there is genetic distance between Black Africans and Eurasians. But this only shows that genetic clusters of human populations do not satisfy half of (a). Hochman (2013, p. 348) uses genetic clustering results from Sarah Tishkoff et al. (2009) to show that there is more genetic structure among Black African populations than among populations at any level of genetic clustering that Black Africans arise as a genetic cluster. > But before I discuss Tishkoff et al.’s results, I should stop and quickly clarify something. It is important to note that ‘genetic diversity’, ‘genetic distance’, and ‘genetic structure’ are noninterchangeable technical terms for Hochman that (roughly) correspond to what Jonathan Kaplan and Rasmus Winther (2013) have called ‘‘genetic diversity’’, ‘‘genetic differentiation’’, and ‘‘genetic heterozygosity’’, respectively, which are three distinct ways of measuring genetic variation. According to Kaplan and Winther (2013, p. 404), genetic diversity is ‘‘a measure of how heterogeneous a system is [genetically].’’ So, for example, p would be a good > example of a measure of genetic diversity.5 In contrast, genetic differentiation > is ‘‘a measure of how different two things are [genetically],’’ and is exemplified by genetic distance calculations, such as Fst genetic distance (Kaplan &Winther, 2013, p. 404). Finally, genetic heterozygosity is ‘‘a measure of the fraction of heterozygotes (as opposed to homozygotes) in a population,’’ and is exemplified by Sewell Wright’s F-statistics or the U-statistics of AMOVA (Kaplan & Winther, 2013, p. 405). With that clarification behind us, we can return to Tishkoff et al.’s results. Tishkoff et al. (2009) used Structure, principle component analysis (or ‘‘PCA’’),6 1327 genetic markers, 3945 individuals, and 181 human populations from all across the globe. Using Tishkoff et al.’s results, Hochman points out that Africans have an incredible amount of genetic structure. Tishkoff et al. (2009) identified 14 genetic clusters of African populations (including Afro-Americans). Just as interesting is that when looking at the worldwide sample, Tishkoff et al. > (2009, p. 1038) found that at KP 4, Black Africans split into different > lusters! For example, at K = 5, the clusters were Caucasoids, Mongloids, Western and Central Africans (including Afro-Americans), Eastern Africans, and the Hadza people of Tanzania.7 Just from looking at these results, it is no wonder why Hochman concluded that genetic clusters of human populations do not satisfy (a)… > > As for (a), genetic distance (or structure) need not be greater among two or more clusters of populations than genetic diversity (or structure) is within any cluster of the set because, again, this condition need not hold in order to have population structure. In fact, Yu et al.’s results are exactly what we should expect for Homo sapiens. Since our species has spent much more time in Africa (P140,000 years) than it has outside of Africa (660,000 years), our species has had a long time to develop a considerable amount of genetic diversity and genetic structure in Africa (Cavalli-Sforza & Feldman, 2003, p. 270). Given this historical reality, we should not expect to find as much genetic diversity or genetic structure outside Africa as we find inside Africa. This, of course, does not imply that humans do not have population structure along (roughly) continental boundaries, since Black Africans, on average, could still be more likely to mate with other Black Africans than with non-(Black Africans). With that said, Tishkoff et al.’s results are concerning because we should expect B to arise at K = 5 if B is a human population partition. > > However, once one examines Tishkoff et al.’s sampling scheme, one will find that Tishkoff et al.’s results are non-threatening to Rosenberg et al.’s results. This is because Tishkoff et al. (2009) dramatically oversample African ethnic groups. African ethnic groups make up 65.1% of Tishkoff et al.’s sample, even though African ethnic groups make up just 30.2% of human ethnic groups.16 Combined with the known fact that most K = 5 human genetic variation lies within parts, not among them, it is unsurprising that a study that greatly oversamples one major geographic region will find that its ethnic groups split into different genetic clusters at K = 5. In fact, Tishkoff et al.’s result is not unique. Friedlaender et al. (2008) sample human populations in such a way that Oceanian ethnic groups make up 48.6% of the sample, even though Oceanian ethnic groups make up just 18.5% of human ethnic groups.17 At K = 5, Friedlaender et al. (2008, p. 178) find that the partition consists of Caucasians, non-Oceanian Mongloids, Black Africans, and two distinct clusters of Oceanians! Of course, neither Tishkoff et al.’s nor Friedlaender et al.’s results conflict with the standard result that K = 5 human genetic clusters are Amerindians, Black Africans, Caucasians, East Asians, and Oceanians, because their samples of human ethnic groups are not appropriate for identifying worldwide human population structure. Rather, these samples are > ppropriate for studying African population structure and Oceanian population structure, respectively. (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,. > [@](#): > > (3) Denial of the history of white supremacy in the United States as way to minimize the likelihood that so-called “nurture” factors explain outcome disparities here. Which is why 1st and 2nd generation Black immigrants do so well on the same measures, right? ---
**Author:** ![Chuck11](https://avatars.discourse-cdn.com/v4/letter/c/96bed5/32.png) [@Chuck11](https://boards.straightdope.com/u/Chuck11)\ **Post date:** [August 19, 2014, 9:39pm UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/214 "2014-08-19T21:39:45Z")
> [@Richard\_Parker](#): > > Let’s see if I understand. So the software looks at a whole bunch of SNPs (not targeting any particular genes necessarily), and then comes up with some assessment of genetic similarity between two individuals based on similarity of SNPs. The more variation in the sampled SNPs, the more the two individuals can be assumed to be genetically distant. > > It then looks to some kind of phenotypic similarity–say, thigh circumference–and estimates the extent to which genetic similarity accounts for the phenotypic similarity. I assume it does some fancy math here to compare how well the genetic variation tracks the phenotypic variation. > > Is that it, or is there something more to it? Because if that’s it, I don’t think it does what you’re claiming. That’s it. And the claim (repeated, not originated by me) is that it establishes the lower bounds narrow heritability. ---
**Author:** ![Chuck11](https://avatars.discourse-cdn.com/v4/letter/c/96bed5/32.png) [@Chuck11](https://boards.straightdope.com/u/Chuck11)\ **Post date:** [August 19, 2014, 9:44pm UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/215 "2014-08-19T21:44:56Z")
> [@Belowjob2.0](#): > > There’s ongoing inquiry into this phenomenon: > > [Epigenetics and IQ variability | For what they were... we are](http://forwhattheywereweare.wordpress.com/2012/10/18/epigenetics-and-iq-variability/) > > [Genome-Wide DNA Methylation and Gene Expression Analyses of Monozygotic Twins Discordant for Intelligence Levels](http://www.plosone.org/article/info:doi/10.1371/journal.pone.0047081) That’s interesting because it’s usually said that epigenetics mimics additive genetics, not unshared environment i.e., makes twins similar, not different. ---
**Author:** ![Richard\_Parker](https://avatars.discourse-cdn.com/v4/letter/r/35a633/32.png) [@Richard\_Parker](https://boards.straightdope.com/u/Richard_Parker)\ **Post date:** [August 20, 2014, 12:29am UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/216 "2014-08-20T00:29:06Z")
> [@Chuck11](#): > > > [@Richard Parker](#): > > > > AFAICT, the racist scum assessment comes from a few moves made by the “racialists”: > > > > (1) Defense of the arbitrary separation of people into traditional racial categories instead of more coherent populations. There is no good defense for using Caucasians, Asians, and Africans as genetic populations. > > When you take representative samples – i.e., don’t over-flavor with certain ethnic population – you get results like figure 7 here: Jombart, T., Devillard, S., & Balloux, F. (2010). Discriminant analysis of principal components: a new method for the analysis of genetically structured populations. BMC genetics, 11(1), 94. Generally, black African groups cluster together because there was lots of boom-boom in Africa. Of course, if you load the sample with Black African, etc populations this will distort the results. I’m not sure how that is responsive to my point. You can divide world populations up into two groups or twenty groups or two thousand groups. The more groups you have, the more internally genetically similar they are. The notion of “race” is that there are clear shelfs in the continuum of genetic diversity in three (or maybe four or maybe five, depending on what suits the racialist for any particular argument) groupings that are substantially greater in magnitude than any other divides in the continuum of genetic similarity. But, so far, the data does not prove that claim. I don’t see anything suggesting otherwise in figure 7 of that paper or your lengthy quote. > [@Chuck11](#): > > > [@Richard Parker](#): > > > > (3) Denial of the history of white supremacy in the United States as way to minimize the likelihood that so-called “nurture” factors explain outcome disparities here. > > Which is why 1st and 2nd generation Black immigrants do so well on the same measures, right? I have no idea whether Black immigrants do better on any given measure than African-Americans, nor why Black immigrants would be a meaningful category for analysis. Were you referring to some study in particular? I think what you’re suggesting is that since Black people not from the United States are free from white supremacy (before they get here), we should expect them to perform better than African-Americans if white supremacy affects outcomes. But this logic is bad for at least three independent reasons. First, white supremacy is not a uniquely American phenomenon. Perhaps you’ve heard of South Africa? Second, immigrants are not a representative sample. They tend to be either more highly-motivated and successful than their countrymen, or more oppressed and vulnerable than their countrymen. And third, there is no scientific measure of whether someone is “Black” other than self-identification, which makes little or no sense in this context of world populations. Do most Aboriginal Australians identify as Black? > [@Chuck11](#): > > That’s it. And the claim (repeated, not originated by me) is that it establishes the lower bounds narrow heritability. Where is that claim made? It isn’t made in the article you cited, as best I can tell. And it doesn’t make a lot of sense, in any event. To name one of a half-dozen ways it would be wrong, it would ignore any co-correlations between genotype and nurture. To offer a trivial example, I have no doubt that individuals with the genes for testicular development earn higher wages. But unless I also look to how much those genes co-correlate with social phenomena, then I can’t say much about the boundaries of heritability of earning a high wage. It doesn’t avoid this problem to look at overall genetic diversity. On the contrary, what GCTA seems to be good for is helping to guess whether a trait has a genetic component or not when we haven’t identified a candidate gene. If genetic variation correlates to variation in the trait, it is a good candidate for heritability. But that’s very very different from claiming that GCTA sets a hard boundary for genetic/non-genetic/epigenetic explanations. AFAICT, it does not. ---
**Author:** ![Chief\_Pedant](https://avatars.discourse-cdn.com/v4/letter/c/a6a055/32.png) [@Chief\_Pedant](https://boards.straightdope.com/u/Chief_Pedant)\ **Post date:** [August 20, 2014, 3:15am UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/217 "2014-08-20T03:15:26Z")
> [@Grim\_Render](#): > > Then there is Africa. The gentic diversity in Africa is bigger than the rest of the worlds total diversity. > > It is like someone wanted to compare genetic variations in dog breeds and decided that a reasonable way to group dog genetic diversity was “_Irish Setter_” - “_English Setter_” - “_Gordon Setter_” - “_Irish Red and White Setter_” - and “_Every other dog plus wolves_” > > It is immediatly obvious that these are not fuctional groups of dog genetic diversity. > > If you were to make honest groups of human population based on genetic variety to call “Race”, you’d end up with most of them being African groups. Wades “race” groups is not based on scientific knowledge. They are instead based on the “race” concept of 18th century supremacists and Aryan power groups. > > Thats the point at which I’d leave the book behind as a waste of time. > > On the raised subject of comparisons between African Americans and caucasians, remember that people exchange genes all the time, and most genes don’t cluster. Slavery ended 150 years ago, at which point african immigration to the US will have declined severely. American blacks are a group defined by the presence of a number of the genes that determine skin color. Whether any other genes have flollwed these genes down the generations is hard to say. The thing about “race” is that it is an artificial decision about how to cluster. We could make a thousand races if we decided to do so. But as it turns out, because of the out-of-africa migration, what “race” does (assuming we are talking about the typical modern groupings, as for example, black/white/asian) is cluster gene pools into descendant lines from that migration anchor point, and that migration point–along with some others–does drive some differences in gene frequencies. This idea that the total amount of diversity has anything to do with whether or not gene frequencies vary among races is a totally irrelevant and confused idea. The hot-button questions around race, such as whether or not observed outcomes are the result of genes and not nurture, hinge on a single contention: gene frequencies driving those outcomes differ by race group. Consider “greyhound” and “all other dogs” as two groupings. There are a group of genes whose frequency is markedly different in the greyhound group once you decide those are the two groupings you make. It may be that the groupings themselves are totally absurd. It may be that they are biologically reasonable. But if dogs were able to group themselves as people do, they could have a “greyhound” group and an “all other group.” Within those groups, the dogs who identify as “greyhound” would then clump themselves into a pool that has a different frequency of genes driving some outcomes–speed, perhaps; a typical shape, perhaps. The average speed of greyhounds would differ from the average speed of “all other dogs” and the reason would be the average difference in gene pools, even if “all other dogs” had a thousand times the amount of diversity and even if the division itself were felt to be arbitrary. What drove that gene frequency? Well at some point the greyhound progenitors were isolated from “all other dogs” to an extent long enough to drive gene frequency differences, and the self-identified association with either “greyhound” or “all other dogs” would accurately enough reflect that history for the gene frequencies to drive average outcomes. It is well-accepted current science that at approximately the L3-M/N split around the time of the (main) out of africa migration 60-ish kya, descendant M/N lines populated most of the rest of the world, and early on (say, 40-ish kya) probably absorbed some archaic lines via Neandertal and Denisovan gene introgression. Those genes are still well-represented in eurasian pools; not so much in sub-saharan pools because gene flow has not been so diffuse that every race is equally homogenized with every other race’s pool of genes. If you do some reading in population genetics and paleoanthropology, you’ll begin to get a feel for how commonly accepted all of this is. You’ll see very common and very casual references to “african” (sub-saharan) and “non-african” frequencies for genes like archaic line genes; post L3/M-N genes like MCPH1 and so on. You will also see plenty of references to the relative frequency of other genes, such as the fact that 90+ % of sub-saharans carry a malaria resistance gene (DARC) while less than 5% of everyone else does. Evolution and migration patterns drive gene frequencies; among the divisions for which it is trivially easy to show gene frequency differences is the continental grouping. In particular the continental grouping of sub-saharan africa and eurasian populations is very easy to show (north africa has much more modern gene flow in common with eurasia, but the sahara barrier has been mostly–though not perfectly–intact over long periods of time). People do exchange genes all the time, but not to the point of homogeneity. In the US, a typical average given for self-identified blacks is close to 20% european ancestry (and blacks in the US over-represent certain west african lines in particular). For self-identified whites, it is probably less than a few percent recent african genes. Many many genes do cluster by self-identified group; so many that some studies which use self-identification for race group, and microsatellite DNA/SNP clustering for continent of recent origin show almost perfect correlation. Those types of studies are done in an effort to decide whether or not self-identification is a reasonable way to approach race-based medicine (short answer: it’s a crude proxy, but individual genomics will shortly supplant it). I hope this helps. It’s a common misperception that the argument about diversity has anything to do with an argument about whether or not “races” have average differences driven by genes. And ultimately the sensitivity about “scientific racialism” is more or less about that second question: do we see different race-grouped outcomes because of the effect of nurture alone, or because gene differences play a major role? Diversity has absolutely nothing to do with that question. If I took a group of very very tall people drawn from all peoples, the outcome difference for height between them and everyone else would be genetic, on average, even if both groups otherwise had huge–or completely different–amounts of genetic diversity for everything else. I hope this helps you think through this. ---
**Author:** ![Chief\_Pedant](https://avatars.discourse-cdn.com/v4/letter/c/a6a055/32.png) [@Chief\_Pedant](https://boards.straightdope.com/u/Chief_Pedant)\ **Post date:** [August 20, 2014, 3:34am UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/218 "2014-08-20T03:34:28Z")
> [@Richard\_Parker](#): > > I’m not sure how that is responsive to my point. You can divide world populations up into two groups or twenty groups or two thousand groups. The more groups you have, the more internally genetically similar they are. The notion of “race” is that there are clear shelfs in the continuum of genetic diversity in three (or maybe four or maybe five, depending on what suits the racialist for any particular argument) groupings that are substantially greater in magnitude than any other divides in the continuum of genetic similarity. But, so far, the data does not prove that claim. I don’t see anything suggesting otherwise in figure 7 of that paper or your lengthy quote. Self-identification into races does create a bifurcation of outcomes in two commonly observed areas: sports and quantified tests such as psychometric evaluations or academic tests. Current data shows no effect on eliminating that gap by equalizing socioeconomic status, and the official position of most scientists and position papers (see, for example, the position paper on race and IQ from the American Psychological Association) is that while there is no evidence for genetics, the gap remains a “mystery.” The argument for substantial race-based outcome differences because of genes has been discussed ad nauseum on this board, but I think it would be safe to say that the magnitude of those black/white/asian gaps is substantial, and given the failure of socioeconomic status or educational opportunity to eliminate the gap, is advanced by non-egalitarians as indirect evidence that the “shelves” for genetic continuum are there at a race level, even if any two populations are trivially clinal. ---
**Author:** ![rsa](https://avatars.discourse-cdn.com/v4/letter/r/839c29/32.png) [@rsa](https://boards.straightdope.com/u/rsa)\ **Post date:** [August 20, 2014, 3:45am UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/219 "2014-08-20T03:45:17Z")
> [@Chief\_Pedant](#): > > (penultimate post before this one) > > [snip] > > I hope this helps you think through this. I can’t speak for anyone else, but it was very helpful to me after several posts where I was losing track and getting glassy eyed. Thanks. ---
**Author:** ![Chuck11](https://avatars.discourse-cdn.com/v4/letter/c/96bed5/32.png) [@Chuck11](https://boards.straightdope.com/u/Chuck11)\ **Post date:** [August 20, 2014, 3:59am UTC](https://boards.straightdope.com/t/at-what-level-is-racialism-accepted-in-the-scientific-community/695257/220 "2014-08-20T03:59:46Z")
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