Category: Uncategorized (Page 1 of 2)

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 F_st 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 F_st  =.111 from Bird (2021; Table 1; 1301 clumped EA SNPs)

Note: H² = broad-sense heritability; r =  intraclass genetic correlation; r_c = intraclass genetic correlation corrected for mathematical constraints on F_st; 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.

 
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).

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.

–Rich, B. E. (1936). A Study of the Relation Between Degree of Indian Blood and Specific Tribe and the Intelligence and Scholastic Marks of the American Indian (Doctoral dissertation, University of Kansas, Education).

–Jonasson, I. (1937). The Comparative Intellectual Abilities of Full and Mixed Blood Indians. MS, University of North Dakota.

–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).

–Comeau, P. J. (1978). A Comparative Study of Academic Achievement of Full-blood and Mixed-blood Indian Students (Doctoral dissertation, University of North Dakota).

–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.

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.
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Thought criminal extraordinaire, Steve Sailer commented recently on Foreign Policy’s article, “Brazil’s New Problem With Blackness.” Money quotes:

These policies didn’t eliminate race, but they did affect how it came to be classified. The marker of race drifted away from a binary consideration of a person’s ancestry and became increasingly based on one’s appearance.
…
What ultimately binds these definitions together is an awareness that the less “black” a person looks, the better — better for securing jobs, better for social mobility. The widespread acceptance of multiracial identities in Brazil coexists with steep racial inequality — a contradiction that the sociologist Edward E. Telles has called “the enigma of Brazilian race relations.”
…
Eleven experts comprised the panel, among them UFPel administrators, anthropologists, and leaders in the wider black community of Pelotas. They received strict guidelines from the Public Prosecutors Office: “Phenotypical characteristics are what should be taken into account,” read the instructions. “Arguments concerning the race of one’s ancestors are therefore irrelevant.”

And this:

“In Aug. 2016, after it had become clear that the law left room for fraud, the government ordered all departments to install verification committees. But it failed to provide the agencies with any guidance.

The Department of Education in Para, Brazil’s blackest state, attempted to fulfill the decree with a checklist, which leaked to the press. Among the criteria to be scored: Is the job candidate’s nose short, wide and flat? How thick are their lips? Are their gums sufficiently purple? What about their lower jaw? Does it protrude forward? Candidates were to be awarded points per item, like “hair type” and “skull shape” …

But black activists say such measures are unavoidable.

When you allow your national policies to be guided by sociological theories, like those of Telles, you are bound to run into this type of mess.

Below are regression results, based on the Pelotas Birth Cohort (n = ~ 2850), for genetic racial ancestry, interviewer and interviewee-reported color (corr), and three SES indicators. In this 1982 birth cohort, independent of European ancestry, it can be seen that there is no consistent negative association between interviewer rated “black” appearance and outcomes. That is, in Brazil, the average race of one’s ancestors is more relevant than stereotypical race-associated phenotypic characteristics. (Note: the sample sizes for “Yellow” and “Indigenous” were small, so those estimates are fairly unreliable; also, neither an East Asian nor Amerindian ancestry component was included).

(Source: F. Hartwig, personal communication, March 4, 2016; full results)

So, if one is interested in addressing historic race-related inequalities, it would be more efficient and just — since (dis)advantages are mostly being passed along lines of descent — to positively discriminate according to objectively determinable biogeographic ancestry, not subjectively assessed stereotypical racial appearance. And it’s hard to see how requiring 23andMe reports would be more intrusive than having a 12 member panel examine applicants for nose width, lip thickness, craniofacial morphology, etc. to see if they are sufficiently African-looking.

Of course, this isn’t going to happen any time soon, since the conclusion that ancestry with respect to major racial or descent groups is relevant to social outcome needs to be evaded, even at the expense of good science and quality social policy.

Kirkegaard, E.O.W., Wang, M., & Fuerst, J. (2017). Biogeographic Ancestry and Socioeconomic Outcomes in the Americas: A Meta-Analysis. The mankind quarterly, 573(3):398-427

It took a particularly long time to publish, owing to the shenanigans we ran into. For example, the editorial board of Frontiers in Genetics reversed their decision (September 12, 2016; affirmed: October 12, 2016) two-three months after deciding to accept with “moderate revision” (July 5, 2016) and mid-review on the grounds that a request from a reviewer “was not satisfactorily met.” What specific request did we brazenly question?

Reviewer 1, round 1: “The discussion of cognitive ability differences across SIREs feels out of place and innappropriate. This paper makes no attempt whatsoever to investigate cognitive abilities, and this discussion should be removed.”

Reply to reviewer 1: “Following the advice of another reviewer [who approved the paper] we added a diagram (Figure 8) to clarify the relevant discussion. Since that reviewer asked for a model and since cognitive ability seems like a plausible pathways to us, we feel that it would be intellectually dishonest on our part to not include the variable. The reason for the present reviewers objection is not clear to us. We do not investigate colorism, yet no objection is made regarding our mentioning of this as a potential mediator of the BGA x SES associations…”

They should have let it slide, because now we feel obliged to prove the point. And prove it again and again, if needs be.

According to one popular version of the race narrative, natural scientific concepts of race were conceptualized, in the 18^th to early 20^th century, such to imply discrete categories; and human “races,” were, accordingly, imaged to have significant discontinuities until post-World War II anthropologists, such as Frank Livingstone (1962), came to realize that human variation was relatively continuous, a fact which, the story goes, demonstrated that human “races,” as traditionally understood, did not exist — instead, only “populations” do. Anyone sufficiently familiar with actual 18^th to early 20^th century discourses on the matter, would find this tale outlandish. They would recall, for example, Wallace’s (1864) account, in “The origin of human races and the antiquity of man deduced from the theory of natural selection,” of the competing pre-evolutionary views about human variation:
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Science is replete with fake, whiggish histories peddled to bolster new paradigms. Biology is no exception. Two examples are the The Essentialism Story (Winsor, 2006; Richards, 2010; Wilkins, 2013) and The Classic View/The Mutationism Myth (Stoltzfus, 2010; Stoltzfus and Cable, 2014). According to the former, early biologists were inexplicably caught in the thrall of Platonic-Aristotelian typological essentialism, which resulted in the failure to recognize the significance of individual variation and which consequently retarded the recognition of evolution. According to the second, early geneticists were caught in the grip of saltationism, which resulted in the rejection of natural selection and held back for decades the synthesis between Mendelian principles and evolutionary theory. As expected, in these tellings, the actual historical views are often barely recognizable.

The most prominent, yet least discussed, example of pseudohistory of science has to be what should be called The Race Narrative. The Race Narrative is meta-myth, comprised of several related tales, which typically involve some permutation of: “”Race” never described a classification which had a proper place in natural history or a classification which, given how it was historically understood, was applicable to humans, but rather was a political construct imposed to oppress certain human groups, which was then back rationalized by natural historians, who read reality through the political ideology of their times.” Often The Essentialism Story and, to a lesser extent, The Mutationism Myth are incorporated into this Narrative.

To give just a few examples:
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After some deliberation, I determined that the locution “race” is inessential. As such, I now disavow the arguably controversial view that this is necessary when it comes to understanding biological variation, human and otherwise…. At the same time, it has become evident that the concept which I refer to as “lineage population,” which I hitherto called “natural division,” a concept which corresponds with Darwin’s “communities of descent,” as understood in On the origin of species by means of natural selection, or the preservation of favoured races is indispensible. I clarify that concept and discuss it in relation to other systematic ones.

Lineage population: A concept needed by an observer of nature? Preprint.

Abstract: The genealogy-based classificatory programs of Kant and Darwin are briefly discussed for context. It is detailed how in biology there is no unambiguous term to reference infraspecific-level descent-based divisions. The term lineage population is introduced and defined for analytic purposes: a lineage population is one of a set of divisions of intrafertile organisms into which members are arranged by propinquity of descent. It is argued that the lineage population concept avoids the ambiguities associated with related biological and anthropological concepts and polysemes such as population, ethnicity, and race. Other terms and concepts, such as form, cline, cluster, geographic population, breeding population, genetic population, breed, species, subspecies, ancestry, geographic ancestry, biogeographic ancestry, ancestral population, ancestry population, natural division, and population lineage, are discussed in relation to this concept. It is concluded that the lineage population concept is a useful analytic tool which picks out, in line with the Kantian/Darwinian perspective, an interesting class of biological variation.