# Human Varieties

Gregory Connor and I submitted the paper, “Linear and partially linear models of behavioral trait variation using admixture regression,” to MDPI’s Behavioral Sciences. This is a methodological paper explicating & proposing some modifications to the frequently used – across hundreds of papers – admixture regression method. We illustrated this method and our proposed tweaks using the ABCD cohort. This manuscript was peer-reviewed by three reviewers, accepted, proof-edited, paid for, but not published. Breaking with MDPI’s clearly outlined protocol, the editor of Behavioral Sciences – who I am fairly sure has now blacklisted me — sent it to a mysterious and seemingly not particularly acute 4th “reviewer”. This “reviewer” argued that the paper was “racist” and based on an “outdated” method. We were not given a chance to respond. And the opinions of the original three reviewers, whom we patiently replied to and made revisions for, were discarded.

You might wonder whether this 4th “reviewer” caught a serious methodological error – or even a substantive one. Nope. Instead, he argued that admixture regression – frequently used, since the early 2000s by numerous geneticists, genetic epidemiologists, medical researchers, and so on – is an “outdated approach (more of the 19th century)”. He kept repeating that the paper was about an outdated “biological concept” of race, when it concerned the relation between traits, genetic ancestry, and self-identified race/ethnicity. To note, typical MDPI reviews are not this ill-conceived and incoherent.

To let you judge if this post-hoc “review” had any merit, I provided this full comment along with my point-by-point empty-chair reply. Since the paper already passed peer-review and was accepted by MDPI, but not published for obvious political reasons, Greg and I have decided to publish it as a chapter in a forthcoming book. I usually do not publish reviews. However since I do not plan to have this paper peer-reviewed yet again, publishing the post-hoc commentary is warranted. Moreover, I usually do not speculate on motives, but it should be noted that, according to the editor, our post-hoc commenter was a knowledgeable geneticist. That fact, with the implication that the commenter understood the technique and literature, suggests that this was a hit job, with the goal of simply persuading the editor to cancel the paper. On the other hand, the commentary does read as if the “reviewer” was either clueless or was just trying to rationalize moral outrage.

“Peer-review” #4.

R4: Connor and Fuerst (here, C&F) proposed a new test that measure how differences in racial identity affects trait variation. They apply their variable to neuropsychological data collected by the Adolescent Brain Cognitive Development (ABCD) study and report that there exists a genetic component to neuropsychological traits and that there is a variation in the performance between different racial groups.

Empty chair reply: As we clearly explained in the introduction, admixture regression is commonly used in genetic epidemiology. Over the last two decades, hundreds of papers have been published using this technique by hundreds of well published geneticists, genetic epidemiologists, medical researchers and so on. In this paper, we explicate the underlying statistical model and propose some improvements to this frequently used technique.

R4: I found this paper unfounded, misleading, dishonest, and outdated, i.e., racist.

Empty-chair reply: Did you get your 30 pieces of silver for this hit job?

R4: The authors are missing some important advances in the field of population genetics. They used outdated terms (races) and cite no literature to support their racial perception.

Empty chair reply: You clearly did not understand the paper. We explicitly contrasted self-identified race/ethnicity (SIRE) with genetic ancestry. The former is posited as tagging environmental effects while the latter is posited as tagging genetic effects: Thus, we note: “Admixture regression leverages these two data sources, self-identified race or ethnicity (SIRE) and genetically-measured admixture proportions, to decompose trait variation correspondingly.” In line with ASHG (2018) we contrast self-identified race/ethnicity, a social construct, with genetic ancestry, a genetic construct. As ASHG (2018) notes:

Although a person’s genetics influences their phenotypic characteristics, and self-identified race might be influenced by physical appearance, race itself is a social construct. Any attempt to use genetics to rank populations demonstrates a fundamental misunderstanding of genetics. The past decade has seen the emergence of strategies for assessing an individual’s genetic ancestry. Such analyses are providing increasingly accurate ways of helping to define individuals’ ancestral origins and enabling new ways to explore and discuss ancestries that move us beyond blunt definitions of self-identified race. [Emphasis added]

R4: Their assumptions about human races are from the previous century. They consistently imply that their usage of racial categories used in social sciences have genetic merit, that’s racism and, of course, wrong. It is not surprise that they cannot find papers to support their genetic model, because it is unfounded.

Empty chair reply: See above. Also, we cited a plethora of examples of papers using admixture regression in the introduction and conclusion.

R4: The authors model individuals as races + admixture, but the emphasis is on races, as admixture is simply defined as combination of more than 1 race. This is a very ignorant modelling of human populations that ignores the vast literature on the subject. The genetic analyses results are skewed to reproduce their perceived racist model.

Empty chair reply: No. Genetic ancestry is not a combination of more than one SIRE group. And there are literally hundreds of papers which employ admixture regression analysis using the same major ancestry groups we used. The ABCD consortium, itself, even has their own genetic ancestry variables (European, African, Amerindian, and East Asian ancestry). We only recomputed these so to include South Asian ancestry

R4: Throughout the manuscript, the authors omit results (i.e., graphs and code) necessary to evaluate their code.

Empty chair reply: We provided the code in the supplemental files. Either you did not check or the editors did not forward this to you.

R4: 1. Where is the support to: “Many diverse national populations descend demographically from isolated continental groups within a few hundred years.”? where did you get it from? where is the scientific reference? ancient DNA study show that mixture is the norm rather than the exception.

Empty chair reply: Admixture within continental groups obviously doesn’t preclude isolation between them.

R4: 2. “Modern genetic technology can measure with high accuracy the proportion of an individual’s ancestry associated with these continental groups.” – yes, modern tests can predict continental origins with high accuracy, but where is the citation?

Empty chair reply: This is from ASHG’s positional statement on this topic.

R4: 3. “In many culturally diverse nations, most individuals can reliably self-identify as members of one or more racial or ethnic groups.” – nonsense. All self-reports are biased. No serious study uses self report ancestry. Of course, the authors must believe in that, because their entire method rests on this connection, but it is untrue. Unlike this unsupported claim of the authors, there are plenty of papers that prove otherwise :
Self-reported ancestry may not be a reliable method to reduce the possible impact of population stratification in genetic association studies of outbred populations, such as in the United States.
https://pubmed.ncbi.nlm.nih.gov/8761246/
https://pubmed.ncbi.nlm.nih.gov/10797159/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2350912/
Read: https://www.nature.com/articles/s41408-018-0132-1 to see the differences between self-reported ancestry and genomic ancestry, calculated very accurately.

Empty chair reply: We did not say that SIRE is a reliable index of genetic ancestry – after all, the whole method is based on the contrast between SIRE and genetic ancestry. Rather, we said that SIRE is a reliable index of itself, in the sense that people who identify as a particular SIRE group at one time identify the same way at another. Thus it reliably tracks a cultural-environment.

R4: 4. Poor modeling: How can self-identified people report their % of ancestry? Hardly anyone mixed is 50%:50%.

Empty chair reply: How much did you bother to read beyond the abstract?

R4: 5. “The genotyped DNA samples are carefully decomposed into admixture proportions of geographic ancestry” – no. they are decomposed into a mixture of racial groups that the authors created after forcing the genetic data to show races. Races and admixture are two different concepts.

Empty chair reply: Translation: “The authors computed genetic ancestry in a standard way and entered this in a regression model with SIRE as have so many other researchers. This is bad: Reasons.”

R4: 6. “In most applications of admixture regression, individuals’ racial or ethnic group identities will have statistical relationships with individuals’ genetically identiﬁed geographic ancestries” – No! where is the evidence? Why this paper is completely devoid of reference for any fundamental assumption of the model. What does it mean “statistical relationships”?

Empty chair reply: Yes! Self-identified race/ethnicity generally, but imperfectly correlates with genetic ancestry. This just restates ASHG’s (2018) positional statement. But since you don’t even understand the meaning of “statistical relationship” what can one expect?

R4: 7. “The objective of admixture regression is to decompose trait variation into linear components due to genetic ancestries and linear components due to racial/ethnic group related effects” – unlike admixture mapping techniques, which the author misleading cite as a parallel method, their method is not designed to link a loci with a trait, but rather link conditions with races with a biological support to the racial concept.

Empty chair reply: Whew!… admixture regression analysis is not ‘our’ method. And this frequently used method is not “designed” to provide “biological support to the racial concept”: it explicitly takes advantage of social constructive aspects of racial identification in admixed populations. Do you need this point illustrated with a crayon?

R4: 8. “We show that the admixture regression model can be viewed as a statistically feasible simpliﬁcation of this linear polygenic index model, in which proportional ancestries serve as statistical proxies for ancestry-related genetic differences.” – proportional ancestries serve as statistical proxies for ancestry-related genetic differences? You calculate ancestries from genetics, this statement means nothing. This is a tautology.

Empty chair reply: So now you finally realize that we used genetic ancestry. But, of course you are still wrong, since local ancestry is a subset of global ancestry. The statement reads: in our model, [global] ancestries serve as statistical proxies for [local] ancestry-related genetic differences.

R4: 9. “an assumption of random mating across ancestral populations” – really? where is the reference for this assumption?

Empty chair reply: Unsurprisingly, no other reviewers had a problem interpreting this statement. To spell it out: It is an assumption made by the theoretical model – thus a limitation – not an assumption about the world.

R4: 10. “A key assumption of the admixture regression model is that admixture arises from recent random mating between the previously geographically-isolated ancestral groups.” – of course no reference, because it is untrue. Your key assumption is not supported by reality.

Empty chair reply:… we restate that random mating is a theoretical assumption of the commonly used admixture regression model which may or may not be violated to a practically significant extent in the real world.

R4: 11. “Many individuals self-identify as belonging to two or more racial or ethnic groups” – you of course model those groups as RACES, by the biological definition, i.e., groups that are completely separate from one another and didn’t mix. Again, where is your evidence (from this century)? Surely you realize that the racial groups that you used do not satisfy this condition, south and east Asians are closer to each other than to Africans, but you ignore that. There are relationships between those groups, it’s not a star topology.

Empty chair reply: We explicitly do not model self-identified “racial or ethnic groups” as “groups that are completely separate from one another and didn’t mix”! If they didn’t mix, we wouldn’t have admixture for our admixture regression! Nowhere in this paper do we talk about “biological races”. We talk about “genetic ancestry” and SIRE. Perhaps you could try reading our actual paper…

R4: 12. The author removed 80% of the genetic data. They claim that they follow the instruction of ADMIXTURE, but there are no such instruction or recommendation.

Empty chair reply: 100,000 random SNPs…. 100,000 random SNPs…

R4:

13. They force the genetic data into 5 racial categories to fit their made up racial categories. They never show a single result of the genetic analyses. we don’t see the STRUCTURE analysis, nor the PCA. We don’t see the scripts that they used. They through populations because they are “overly admixed”?? what does it mean? You think that Hispanics are less admixed than Druze? Where is the evidence? Why everything in this manuscript is made up BS?

Empty chair reply: You mean: we use K=5 (European, Amerindian, African, East Asian, & South Asian) instead of the K=4 (European, African, Amerindian, & East Asian) provided by the National Institute of Health for the ABCD dataset… Yes, only “racists” would use these ancestry components.

R4: 14. The authors don’t report their results. Are they afraid? Where are the findings of the model (blacks are poor and uneducated, bla bla). What is the point of this paper if the authors don’t stand behind their results? Why should anyone believe in it?

Empty chair reply: So you missed the part that this was a methodological paper which then illustrated the methodology using the ABCD sample.

15. Where is the null hypothesis?

R4: 16. I have major ethical concerns due to the extensive use of races, biologically defined. I think that it is wrong and unsupported by the data nor literature.

Empty chair reply: …so, again, we used SIRE vs. genetic ancestry. Which one, exactly, is the “wrong and unsupported” “races, biologically defined”?

R4: Minor comments 1. “It has particular value in the case of complex behavioral traits where reliably identifying genetic loci associated with trait variation is beyond the current reach of science” – so it is not beyond the reach of science?

Empty chair reply: Would you like it to be?

R4: I have a few more comments, but I think that the trend here is pretty obvious. It is an outdated approach (more of the 19th century).

Empty chair reply: Well, maybe you should tell that to the hundreds of research teams that currently use this method.

Thank you so much for your support! We met our yearly fundraising goal within 12 hours of yesterday’s post. We look forward to finishing and publishing these analyses.

In Lasker, Pesta, Fuerst, and Kirkegaard (2019), we found an unstandardized beta for European genetic ancestry, when predicting g, of .85 among African Americans (model 2; Table 6). Simply put: a 100% increase in European (vs. African) ancestry was associated with a 0.85 d increase in intelligence. We interpreted these results as strong support for a partial hereditarian model. As did others in the HBD sphere.

Bird (2021a), in contrast, argued that our regression analyses suffered from omitted variable bias. Notably, he did not disagree that the results would support a hereditarian model were they robust.

Given the 2.053 d (or 30.8 point) measured test score difference between continental Africans and Europeans which Bird (2021a) adopts, genetic effects alone, based on our results, would represent .85 d /2.053 d = 41% of the phenotypic difference. Expressed in terms of variance explained, this would be (.85 d)^2/(2.053 d)^2 = 17.14%. [1] However, this is relative to an average within-groups heritability for g of 66.5% for this specific sample (Mollon et al., 2018; Pesta, Kirkegaard, te Nijenhuis, Lasker, & Fuerst, 2020). Since the expected differences are proportionate to the within-groups heritability, the variance explained would be predicted to be around 17.14%/66.5%*50% = 12.88% conditioned on a heritability of 50%.[2]

Now, based on his analysis of SNP data, Bird (2021a) estimated a variance explained of 12% given a heritability of 50%. Thus, these two very different methodologies (global admixture analysis & SNPS Fst comparisons) derive very similar estimates conditioned on the same heritability coefficient.[3]

But Bird (2021) goes on to interpret his result as “no support for a hereditarian hypothesis”. Well, one could define a ‘hereditarian hypothesis’ such that these magnitudes do not support it. But, in that case, one could just cite our own widely discussed research results against it. In this case, Bird (2021b) should then also state that, “Lasker et al. (2019) also found ‘no support for the hereditarian hypothesis of the Black–White achievement gap’ and, in fact, Fuerst is strongly supportive of an environmental model, despite what some disreputable sites claim.”

I won’t complain. I am sure that being labeled an environmentalist will not hurt my career prospects. However, don’t call me a hereditarian for arguing X but then go on to argue X and also call that ‘no support for a hereditarian hypothesis’.

Note:
[1] To convert between variance metrics, such as R^2, and linear metrics such as r, you take the square-root of the former or the square of the latter. The difference between variance and linear metrics can lead to misinterpretations, since variance metrics do not align with our intuitive sense of distance. Phil Birnbaum (2006) gives the following example: if you were playing baseball and you made it to second base, you might think you made it 2/4 = .5 or one-half of the way home, but in terms of variance metrics you really only ran 2^2/4^2 = 4/16 =.25 or one-quarter of the total variance to home base. This is why, in context to the continental African and European differences discussed, a between-group variance of 17.14% is equivalent to a real-world percent explained of sqrt(17.14%) = 41%.

[2] Originally, I reported an average heritability for g in the TCP sample of 81.5; the correct value was 66.5 (White = 72%; Black = 61%). The text has been updated.

[3] As for which estimates to use, a point which Bird (2021b) touches on, ideally one would employ both within-groups broad-sense heritability and total genetic variance between populations so to calculate the broad-sense between-group heritability and the total expected differences. This is insofar as one is interested in the overall differences, not predicting offspring values from parental ones or testing specific evolutionary models. Now Bird (2021a) cites Polderman et al. (2015). For adults (age 16 to 65), Polderman et al. (2015) give meta-analytic MZ and DZ correlations of .68 and .28 (Figure 3; High-level cognitive functioning), which, using Falconer’s formula, yields a meta-analytic broad-sense heritability of 80%.

Of this, most of the variance is additive genetic; nearly all the remainder is due to an unknown mix of active gene-environmental covariance and dominance variance. Now, if for methodological or theoretical reasons, one uses within-groups narrow-sense heritability and additive genetic variance between populations, one simply derives the expected differences due to additive genetic differences. That can be useful for certain purposes, however, it will underestimate total genetic differences (unless, unexpectedly, in this case, the genetic variance components go in discordant directions between populations). Regardless, since global admixture results will relate to broad-sense heritability, one needs to adjust the heritability when comparing the results of Bird (2021) to those of Lasker et al. (2019).

References
Bird, K. A. (2021a). No support for the hereditarian hypothesis of the Black–White achievement gap using polygenic scores and tests for divergent selection. American Journal of Physical Anthropology.
Bird, K. A. (2021b, February 12). Still No Support For Hereditarianism. Accessed at: https://kevinabird.github.io/
Lasker, J., Pesta, B. J., Fuerst, J. G., & Kirkegaard, E. O. (2019). Global ancestry and cognitive ability. Psych, 1(1), 431-459.
Mollon, J., Knowles, E. E., Mathias, S. R., Gur, R., Peralta, J. M., Weiner, D. J., … & Glahn, D. C. (2018). Genetic influence on cognitive development between childhood and adulthood. Molecular psychiatry, 1-10.
Pesta, B. J., Kirkegaard, E. O., te Nijenhuis, J., Lasker, J., & Fuerst, J. G. (2020). Racial and ethnic group differences in the heritability of intelligence: A systematic review and meta-analysis. Intelligence, 78, 101408.
Polderman, T. J., Benyamin, B., De Leeuw, C. A., Sullivan, P. F., Van Bochoven, A., Visscher, P. M., & Posthuma, D. (2015). Meta-analysis of the heritability of human traits based on fifty years of twin studies. Nature genetics, 47(7), 702-709.

It’s March!

Which means that the Human Phenome Diversity Foundation’s (HPDF) annual fundraising drive has commenced.

Our goal is $2,500. We have some great projects which we would like to support this year if we can afford to. Last year’s fundraising helped finance an important admixture paper, currently under review, which is up at biorxiv. We would like to continue to fund genetically informed research with your support. If you care to see this research done, you can donate at the HPDF’s official gofundme charity site. Donations are tax-deductible since the HPDF is a 501(c)(3) organization. Also, the HPDF now has an associated corporate Kraken account, so you can donate directly with cryptocurrencies, too: Bitcoin(XBT):34fHxYLwEVEpcn7GLLuYtZ4PZcZp9qWbhA Ethereum(ETH):0x53d65c5f757D59153Cf9fffC44D40989FCcFB602 Monero(XMR):83SiAyTG7GdE5uvUuDj61SKmAQhHXuuxE5EKP3kao5GMiveZf 3oLSbsgc5Pejk5PajQjGVUF6YV11ZQbEWikJFxX2tRgX9R Kevin Bird has a paper out in which he claims, more or less, to evidence “insignificant” race differences. There is a lot there to criticize: misinterpretations, odd analytic choices, a crucial wrong formula [1], etc. Maybe I will write a formal critique. For now, it’s sufficient to point out that the results strongly agree with a hereditarian model: • The predicted differences, given the genetic divergence in the educational and intelligence SNPs, are medium to large given reasonable estimates of broad-sense heritability (H2)[2]. • While there is inconsistent evidence of divergent selection (for this pairwise comparison), there is zero evidence of homogenizing or stabilizing selection. To illustrate point (1), Table 1 shows the expected BGH given the 30.8 point continental European-African difference which Bird adopts along with the expected phenotypic gaps when environments are equal (i.e., when BGH is set to unity). I use the lowest Fst value Bird reports in his table. Proofs are provided for the formulas used in the .doc file. Table 1. Expected Between Group Heritability (BGH) and Expected IQ Point Differences between Europeans and Africans Given Different Values of the Genetic Intraclass Correlation (r and r_c) and H2 assuming an eduSNP Fst =.111 from Bird (2021; Table 1; 1301 clumped EA SNPs)  H2 r t_observed BGH t_expected Expected IQ difference Cohen’s Interpretation 0.20 0.1990 0.5132 0.047 0.0473 6.69 Medium 0.35 0.1990 0.5132 0.083 0.0800 8.85 Medium 0.50 0.1990 0.5132 0.118 0.1105 10.58 Medium 0.65 0.1990 0.5132 0.153 0.1391 12.06 Large 0.80 0.1990 0.5132 0.189 0.1658 13.38 Large H2 r_c t_observed BGH t_expected Expected IQ difference Cohen’s Interpretation 0.20 0.2844 0.5132 0.075 0.0736 8.46 Medium 0.35 0.2844 0.5132 0.132 0.1221 11.19 Medium 0.50 0.2844 0.5132 0.188 0.1657 13.37 Large 0.65 0.2844 0.5132 0.245 0.2053 15.25 Large 0.80 0.2844 0.5132 0.302 0.2412 16.91 Large Note: H2 = broad-sense heritability; r = intraclass genetic correlation; r_c = intraclass genetic correlation corrected for mathematical constraints on Fst; t_observed = intraclass phenotypic correlation i.e., phenotypic variance between groups (given d = 2.053); BGH = between group heritability; t_expeced = expected phenotypic variance between groups when environments are equalized; Expected IQ difference = expected IQ differences when environments are equalized; Cohen’s Interpretation = conventional interpretation of effects sizes. You can argue that one should use narrow-sense heritability, instead of broad-sense, contra Jensen (1972; 1998), then lowball the estimates, and finally take advantage of statistical illiteracy and portray the differences as ‘small’ or ‘insignificant’ by emphasizing the portion of variance explained. However, the expected differences (which are equal to sqrt(BGH) x observed phenotypic differences) are still medium to large. Of course, Bird (2021) argues that the differences could go either way with equal likelihood. This would be true if you knew nothing else. However, in his prior analyses, he uses polygenic score (PGS) weights, and the eduPGS weights are directional. For the same set of eduSNPs the PGS differences are shown below: Table 2. Mean MTAG-based PGS for CEU and YRI Calculated using population-GWAS and Within Family Betas.  W/ population-GWAS W/ Within Family Betas CEU (N = 99) YRI (N = 108) CEU (N = 99) YRI (N = 108) All SNPS 0.866 -0.794 0.614 -0.563 p-value (Welch’s Two Sample t-test) < 0.0001 < 0.0001 Derived SNPs 0.938 -0.860 0.702 -0.643 p-value (Welch’s Two Sample t-test) < 0.0001 < 0.0001 Ancestral SNPs 0.605 -0.554 0.528 -0.484 p-value (Welch’s Two Sample t-test) < 0.0001 < 0.0001 Note: SNPs were filtered for MAF >0.01 for both CEU and YRI. Scores represent standard scores calculated using the standard deviation in the total sample. Sample sizes for the t-test were N = 99 for CEU and N=108 for YRI. Thus, it makes no sense to say that the expected difference could go either way, with equal probability, when the eduPGS weights indicate a direction. When this is recognized, the only option is to declare that the eduPGS is biased between populations. This is possible, of course. However, this leaves the evolutionary default or null, which is that differences will be commensurate with neutral variation. As Rosenberg, Edge, Pritchard, & Feldman (2019) note: “One key component of the inference of polygenic adaption is the use of an appropriate null expectation for polygenic scores distributions and phenotypic differences…[P]henotypic differences among populations are predicted under neutrality to be similar in magnitude to typical genetic differences among populations.” The authors, of course, go on to cite Lewontin and slyly note that differences “are small in comparison with variation within populations”. But, of course, “large” differences in the conventional sense are also “small in comparison with variation within” (e.g., .80d = 14% variance). And while the evolutionary default is directionless, the totality of the behavioral genetic and psychometric data assembled on this topic points one way. [1] See, for example, equation 4 in Bird (2021). However, total between phenotypic variance = phenotypic variance due to genes + phenotypic variance due to environment which can be rewritten, in linear metrics, as PD^2 = GD^2 + ED^2 or PD = sqrt( GD^2 + ED^2 ) Since, BGH = phenotypic variance due to genes / total between phenotypic variance BGH = GD^2 / PD^2 and, therefore, GD = sqrt(BGH)*PD This is approximated but underestimated by 2*PD^2 * sqrt(2/pi) (*15) which Bird (2021) uses. e.g., sqrt(.12)*30.8 = 10.67 (correct) versus 2*sqrt(.12)*sqrt(2/pi) (*15) = 8.29 (Bird, 2021) [2] While the use of narrow-sense heritability is recommended for Qst-Fst comparisons and the assessment of directional selection, narrow-sense heritability, and the corresponding narrow-sense Qst underestimates between-group genetic variance by not taking into account non-additive genetic variation between populations, along with active gene-environment covariance (which is commonly classed as a genetic effect; Sesardic, 2005). Thus when it comes to calculating the expected difference due to genes, it makes sense to use the broad-sense heritability, at least for an upper-bounds estimate, as hereditarians have done (e.g., Jensen, 1998). In 1969, Harvard Educational Review published a long, 122-page article under the title “How Much Can We Boost IQ and Scholastic Achievement?” It was authored by Arthur R. Jensen (1923–2012), a professor of educational psychology at the University of California, Berkeley. The article offered an overview of the measurement and determinants of cognitive ability and its relation to academic achievement, as well as a largely negative assessment of attempts to ameliorate intellectual and educational deficiencies through preschool and compensatory education programs. Jensen also made some suggestions on how to change educational systems to better accommodate students with disparate levels of ability. While most of the article did not deal with race, Jensen did argue that it was “a not unreasonable hypothesis” that genetic differences between whites and blacks were an important cause of IQ and achievement gaps between the two races. This set off a huge academic controversy—Google Scholar says that the article was cited more than 1,200 times in the decade after its publication and almost 5,400 times by December 2019. The dispute about the article centered on the question of racial differences, which is understandable as Jensen’s thesis came out on the heels of the civil rights movement and its attendant controversies, such as school integration, busing of students, and affirmative action. Jensen questioned whether it is in fact possible to eliminate racial differences in socially valued outcomes through conventional policy measures, striking at the foundational assumption of liberal and radical racial politics. His floating of the racial-genetic hypothesis was what set his argument apart from the general tenor of the era’s scholarly and policy debate. In this post, I will take a look at Jensen’s arguments and their development over time. The focus will be on the race question, but many related, more general topics will be discussed as well. The post has four parts. The first is a synopsis of Jensen’s argument as it was presented in the 1969 article. The second part offers an updated restatement of Jensen’s model of race and intelligence, while in the third part I argue, using the Bradford Hill criteria, that the model has many virtues as a causal explanation. In the fourth and concluding part I will make some more general remarks about the status and significance of racialist thinking about race and IQ.[Note] Continue reading Last updated: 4/18/2018 I was asked to meta-analyze a century (1914-2014) of IQ/Academic achievement and racial admixture (genealogy, gestalt racial appearance, and color) research. There is a lot out there, especially when one takes into account MA & PhD dissertations. To this end I am posting$20 (negotiable) bounties for each of the following dissertations (to be paid in bitcoin):

–Snider, J. G. (1953). A Comparative Study of the Intelligence and Aptitudes of Whites and Nezperce Indians (Doctoral dissertation, University of Idaho).

–Zimmerman, H. E. (1934). The Indian’s Ability to Learn Mathematics According to Degree of Indian Blood. MA, Kansas State Teacher’s College, Pittsburg.

–Rainey, C. D. (1932). A study of the Salem Indian High School, comparing the cultural background, the intelligence scores, and the per cents of white blood, and the classroom grades (Doctoral dissertation, Willamette University).

–Ross, D. D. (1962). A comparative intergroup study of the academic achievement and attendance patterns between the full-blood type and the mixed-blood type Oglala Sioux Indian student in the secondary department of Oglala Community School, Pine Ridge, South Dakota (Doctoral dissertation, Chadron State College).

The full dissertations are not needed, but just a copy (or photo) of the relevant tables and/or correlation matrices along with the following sample characteristics: country of sample, first order administrative unit of sample (e.g., North Carolina), group type (e.g., school, college, random stratified), ethnic group, age range, sample size, description of the ancestry index, cognitive tests used, statistical methods for comparing admixed groups (e.g., means & SD, correlations, Chi-square)

This should be an easy job if you are at one of the schools at which there is a copy of the dissertation. If interested email at j122177@hotmail.com. I will update this list as I go along.

Given the central role that testing plays in the American educational system, most datasets that we have on racial and ethnic differences in cognitive ability include only children, adolescents, or young adults. Most of the economic and social effects of cognitive differences are, however, produced by the working age population, so it would be useful to have test scores from older adults as well. The PIAAC survey of adult skills conducted by the OECD provides excellent data for this purpose. Continue reading

Regression to the mean, RTM for short, is a statistical phenomenon which occurs when a variable that is in some sense unreliable or unstable is measured on two different occasions. Another way to put it is that RTM is to be expected whenever there is a less than perfect correlation between two measurements of the same thing. The most conspicuous consequence of RTM is that individuals who are far from the mean value of the distribution on first measurement tend to be noticeably closer to the mean on second measurement. As most variables aren’t perfectly stable over time, RTM is a more or less universal phenomenon.

In this post, I will attempt to explain why regression to the mean happens. I will also try to clarify certain common misconceptions about it, such as why RTM does not make people more average over time. Much of the post is devoted to demonstrating how RTM complicates group comparisons, and what can be done about it. My approach is didactic and I will repeat myself a lot, but I think that’s warranted given how often people are misled by this phenomenon.

There are a couple of new, well designed, obtainable, surveys out — with ancestry, MRI, and cognitive data – which should allow for the (dis)confirmation of certain conjectures of ill repute:

–Neurodevelopmental Genomics: Trajectories of Complex Phenotypes (age 8-21, N ~ 10,000)
–The Brain Genomics Superstruct Project (age 18-35, N ~ 1,500)

For example, Greg Cochran likes to go on about how major ancestry groups often differ in crude brain morphology, and how these differences probably explain a significant chunk (> 20%) of bio-ancestry related differences in CA. I doubt it. But if he agrees to specify the analytic strategy, I will try to get the data and run the analyses.

I did look through the PING survey (age 3-21, N ~ 1,500) – which might not be very informative owing to the age structure. Going by this, Greg seems to be more or less correct about some of the endo differences and probably about their origins. As an example, Figure 1 & 2 show the B/W diffs for intracranial and total brain volume by age. (AAs are picked out for illustration since they are the largest non-White ethnic group, showing the biggest deviation from Whites.) And Figure 3 shows the relation between brain volume and ancestry in the self-identified AA group; the results were basically the same for intracranial volume, etc. — and so not shown.

Yet, as seen in Table 1 &  2, CA was more or less uncorrelated with these particular endophenotypes (r = 0.07-0.08); unsurprisingly, CA explained virtually no endo differences, and vice versa. Yet, CA was strongly (negatively) associated with both African and Amerindian ancestry – and also, though to a lesser degree, with Oceanian.

Perhaps there is a more sound way to run the numbers? Or a better way to take into account age? Dunno, it’s not my position to defend.

Results below.