Miscegenation
Are We Subject To Outbreeding Depression? Molecular Genetic Evidence
Introduction:
The theoretical basis for expecting mixed-race persons to be lower in genetic fitness outcomes is analogous to the reason that inbreeding results in lower fitness. Inbreeding allows rare, recessive alleles to be expressed which normally never would be. Since such alleles haven't been expressed in previous generations, any such alleles which are deleterious haven't yet had the opportunity to be weeded out by natural selection. Such alleles therefore tend to be much more deleterious than the dominant alleles and the common recessive alleles that are normally expressed.
Analogously, genes don't just evolve in isolation, as they are passed on in sets. The presence of one gene may modify the effect that another gene has on an organism's phenotype. If then, you destroy this context by putting a gene from a bacteria in a human, the gene may not be adapted to the new genetic architecture, and it may have deleterious effects even if the gene was originally built to serve the same physiological cell function when expressed in the bacteria.
Finding molecularly-verified examples of this sort of phenomenon having trait relevance will always be tedious (and politically incorrect, so understudied and unpublished), but we already have a couple of examples:
HapK is very rare in Africa, and only present in Black Americans due to European admixture. It carries a modest risk of myocardial infarction for Europeans, but a threefold-larger risk for Africans [7].
The ApoE4 allele confers less risk of Alzheimer’s disease when present in Blacks than it does when present in Whites [8 & 9].
Instead, it may be more systemically viable to find the raw differences in genomic architecture even if doing so doesn’t tell us the phenotypic implications of such differences. How might we do so?
Gene expression:
Most basically, we may have two alleles (X and Y) for a gene, and two groups (A and B) that the gene can be expressed in. If the groups differ in their propensity to express that gene, then predicting the phenotypic effects of giving allele X to a member of group A instead of allele Y is not as simple as observing the effects of the two alleles in group B. So, the most basic thing we might investigate in our inquiries into whether there are population differences in gene architecture is whether or not the races differ in gene expression. There is evidence that they do:
[1] N = 142: Of 4197 genes tested, 1097 differed in expression between Europeans and Asians at P<.00001, and 27 differed between Chinese and Japanese at P<.00001. With expression phenotypes for the 1097 genes, cluster analysis was also able to correctly identify 165/166 of the individuals in the sample as either European or Asian.
[2] N = 16: Of 5,194 genes tested, 1210 (83%) of genes were found to differ among individuals in gene expression to a statistically significance degree, and 17% were found to differ between europeans and africans to a statistically significant degree.
[3] N = 2,733: "Fine-mapping of expression quantitative trait loci (eQTLs) in individuals with predominantly African or Indigenous American ancestry revealed ancestry-specific eQTLs in over 30% of heritable genes."
Keep in mind for these papers that depending on measurement quality or statistical power, certain differences in gene expression may not be large enough to be counted as a difference in gene expression, and so the percentage of genes where groups differ in gene expression is to be considered to be floored at the estimates that these papers produce.
PGS:
As we all know, the races differ in polygenic scores for intelligence. The validity of these polygenic scores however differ among races [4], although this isn't necessarily a problem for us because we know that PGS gaps remain when corrected for differences in PGS validity. These PGS validity differences could theoretically be due to A) environmental confounding; B) group differences in linkage disequilibrium patterns (see e.g. [5]); or C) group differences in gene architecture which causes the same alleles to have different effects depending on which group the alleles present in. Accordingly, it has been demonstrated in the GWAS literature that population-specific genetic architecture is more easily understood with the use of race/ethnicity information [6]:
Reproduction:
One common argument for why the races can’t be considered subspecies is that they are able to produce fertile offspring. However, there are plenty of species which aren’t completely isolated from each other and which are in gene-flow contact despite still being considered to be separate species [10]. Moreover, incompatibilities which prevent species from hybridizing are actually able to collapse again after they’ve initially formed [11]. How do the races measure up?
Genes involved in biological processes like “pigmentation”, “ melanocyte differentiation”, and “pigmentation during development” are less racially differentiated than are genes involved in biological processes like “gamete generation”, “spermatid development”, and “sperm motility” [12]:
Figure 1 𝛌 values of GO categories in biological processes enriched for higher FST SNPs with P-value lower than 10^-10
Sauce:
Spielman, R. S., Bastone, L. A., Burdick, J. T., Morley, M., Ewens, W. J., & Cheung, V. G. (2007). Common genetic variants account for differences in gene expression among ethnic groups. Nature genetics, 39(2), 226-231. Retrieved from https://sci-hub.ru/https://doi.org/10.1038/ng1955
Storey, J. D., Madeoy, J., Strout, J. L., Wurfel, M., Ronald, J., & Akey, J. M. (2007). Gene-expression variation within and among human populations. The American Journal of Human Genetics, 80(3), 502-509. Retrieved from https://sci-hub.ru/https://doi.org/10.1086/512017
Kachuri, L., Mak, A. C., Hu, D., Eng, C., Huntsman, S., Elhawary, J. R., ... & Ziv, E. (2022). Gene expression in African Americans and Latinos reveals ancestry-specific patterns of genetic architecture. bioRxiv, 2021-08. Retrieved from https://www.biorxiv.org/content/10.1101/2021.08.19.456901v1
Pesta, B. J., Fuerst, J. G., Piffer, D., & Kirkegaard, E. O. (2020). Intelligence-associated Polygenic Scores Predict g, Independent of Ancestry, Parental Educational Levels, and Color among Hispanics in comparison to European, European-African, and African Americans. bioRxiv. Retrieved from https://www.biorxiv.org/content/10.1101/2020.09.24.312074v2.abstract
Carl, N. (2022). Is there "zero evidence" for hereditarianism? Noah’s newsletter. Retrieved from
https://noahcarl.substack.com/p/is-there-zero-evidence-for-hereditarianism
Fang, H., Hui, Q., Lynch, J., Honerlaw, J., Assimes, T. L., Huang, J., ... & Tang, H. (2019). Harmonizing genetic ancestry and self-identified race/ethnicity in genome-wide association studies. The American Journal of Human Genetics, 105(4), 763-772. Retrieved from https://sci-hub.se/https://doi.org/10.1016/j.ajhg.2019.08.012
Helgadottir, A., Manolescu, A., Helgason, A., Thorleifsson, G., Thorsteinsdottir, U., Gudbjartsson, D. F., ... & Stefansson, K. (2006). A variant of the gene encoding leukotriene A4 hydrolase confers ethnicity-specific risk of myocardial infarction. Nature genetics, 38(1), 68-74. Retrieved from https://sci-hub.se/https://doi.org/10.1038/ng1692
Ferrar, L. A., Cupples, L. A., & Haines, J. L. (1997). Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. JAMA, 278, 1349-1356. Retrieved from https://sci-hub.se/https://doi.org/10.1001/jama.1997.03550160069041
Howell, J. C., Watts, K. D., Parker, M. W., Wu, J., Kollhoff, A., Wingo, T. S., ... & Hu, W. T. (2017). Race modifies the relationship between cognition and Alzheimer’s disease cerebrospinal fluid biomarkers. Alzheimer's research & therapy, 9(1), 1-10. Retrieved from https://sci-hub.se/https://doi.org/10.1186/s13195-017-0315-1
Mallet, J. (2005). Hybridization as an invasion of the genome. Trends in ecology & evolution, 20(5), 229-237. Retrieved from https://sci-hub.ru/https://doi.org/10.1016/j.tree.2005.02.010
Xiong, T., & Mallet, J. (2022). On the impermanence of species: the collapse of genetic incompatibilities in hybridizing populations. Evolution. Retrieved from https://onlinelibrary.wiley.com/doi/epdf/10.1111/evo.14626
Wu, D. D., & Zhang, Y. P. (2011). Different level of population differentiation among human genes. BMC evolutionary biology, 11(1), 1-7. Retrieved from https://sci-hub.ru/https://doi.org/10.1186/1471-2148-11-16
I like your content sir, good work. I’m trying to do some research of my own too, in regards to crime, race/ethnicity and immigration. Are there any good statistical resources for ethnicity/race and migrant crime in Germany? I got into a discussion not too long ago with someone who pointed out the unrigorous nature of their crime stats. For example, this person stated that a gang of neo-Nazis committed a string of murders (over a period of 10 years), and that the suspects of the case included migrants (when the real perps were ethnic Germans, but that hadn’t been established yet), thus, “suspect” rates are not the most accurate measurement. For one, I think that’s a very generous extrapolation and assumption on his part (assuming that a bunch of Neo-Nazis are to blame for inflated non-German suspect rates), but I imagine the best way to calculate migrant/non-German crime is to look at conviction rates, prison population, and crimes which involve witnesses/victims, such as sexual assault or rape. That, and the German statistical agencies don’t seem to have ethnic/racial breakdowns for either “non-Germans” or “Germans” (the latter could be a Kurd with German citizenship/nationality, rather than an ethnic German or West European). Their system compared to the US or even the UK, is horrible and myopic to say the least.
most people are racially mixed. It is a mixture of different ancient races. It's easy to understand that Indians and Central Asians are hybrids. But even Europeans, for example, are a mix of very different ancient races. Perhaps this mixture contributed to intelligence and other beneficial psychological traits.
https://www.nature.com/articles/nature13673